Newborn Brains, Big Dogs, Bigger Gaps · Morning Gist
Saturday, October 175 stories · 15 min
Newborn Brains, Big Dogs, Bigger Gaps
Today: a therapy trial that may reach the womb, why habits explain little of the wealth gap in lifespan, and what large dogs show about aging.
Picked from 27 new articles across 12 sources · arrow keys for other days
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In a 234-woman trial, babies born to depressed mothers who got eight therapy sessions had hippocampi about 5% smaller on MRI. story 1 ↓
Over 20 years, a study of 33,541 Chinese adults aged 65+ found habits explain only about a fifth of the rich–poor longevity gap. story 2 ↓
About 7 in 10 Australian children with accounts stayed on banned platforms. No data yet show whether the ban improves their health. story 3 ↓
Among 894 pet dogs, big dogs lost methylation on ancient viral DNA 31% faster with age, pointing to failing gene silencing. story 4 ↓
Medi-Cal has grown from $50 billion to $222 billion a year, and neither candidate for California governor says how he'd cover the federal cuts. story 5 ↓
ACOG has updated its guidance on treating hot flashes, night sweats and insomnia in menopause, the first revision since 2014.
1/5The Conversation: Health· Elysia Poggi Davis, Professor of Psychology, University of Denver· Oct 16
Talk therapy for depressed pregnant women linked to differences in newborn brains
A randomized trial gave depressed pregnant women eight sessions of a brief talk therapy. Their newborns had a slightly smaller hippocampus on brain scans, and smaller volume tracked with calmer infant reactions at six months.
Why it matters · If confirmed, it suggests a cheap, drug-free treatment during pregnancy could affect the child's brain development, which strengthens the case for routine prenatal depression screening and care.
Know this first
Context from the editor, not the article · 26 sec
1 · Depression in pregnancy
Up to 1 in 5 women have depression during pregnancy. It is linked to high blood pressure, preterm birth and higher rates of mental illness in the child. Many affected women get little or no treatment.
2 · Interpersonal psychotherapy
Interpersonal psychotherapy is a short, structured talk therapy. It treats depression by working on relationships, such as resolving conflicts, handling role changes and building support, not by digging into the past.
3 · Why randomize with care
2/5Fight Aging!· Reason· Oct 16
Lifestyle explains only about a fifth of the health gap between rich and poor older adults
In a 20-year study of 33,541 older adults in China, healthy habits accounted for about 20% of the higher death risk in low-status groups. Better-off people gained the most years from healthy living.
Why it matters · If habits explain only a fifth of the longevity gap between social classes, telling poorer people to live healthier leaves most of the gap in place.
Know this first
Context from the editor, not the article · 29 sec
1 · Status and lifespan
Richer, better-educated people live longer and stay healthier in old age, in nearly every country studied. Whether that comes from habits, environment, medical care or something else is still debated, because observational data can't easily separate causes.
2 · What mediation analysis does
Mediation analysis asks how much of the link between an exposure (here, social status) and an outcome (death) runs through a third variable in between (lifestyle). Its answer is only causal if its strong assumptions about confounding hold.
3 · Hazard ratios
A hazard ratio compares how often an event, such as death, happens over time in two groups. An HR of 1.25 means a roughly 25% higher rate in the first group than in the comparison group.
3/5The Conversation: Health· Ari Lightman, Professor of Digital Media and Marketing, Carnegie Mellon University· Oct 16
Early data show teens getting around Australia's social media ban
More than 20 countries are banning or planning to ban social media for minors to protect their mental health. Early Australian data show most teens get around the ban, and a researcher argues for platform safety rules instead.
Why it matters · Governments are making youth mental health policy fast, but the data so far measure whether bans are followed, not whether they make teenagers healthier.
Know this first
Context from the editor, not the article · 25 sec
1 · The Anxious Generation debate
Jonathan Haidt's 2024 book argues that phone-based childhoods drive teen anxiety and depression. Critics note that most supporting studies are correlational, so they can't show that social media causes the rise.
2 · Australia's under-16 ban
Since December 2025, Australia has required platforms such as TikTok, Instagram and Snapchat to keep under-16s off and to verify users' ages. The eSafety Commissioner, the national online-safety regulator, enforces it.
3 · The tobacco settlement precedent
4/5Fight Aging!· Reason· Oct 16
Big dogs' DNA methylation shifts faster with age, especially at viral leftovers
Researchers built epigenetic clocks from 1,640 blood DNA samples from 894 pet dogs. Dogs whose clocks ran ahead of their real age were more likely to die. In large dogs, chemical marks that keep ancient viral DNA quiet wore away faster.
Why it matters · Dogs age and die at very different rates within one species, so they give a natural test of which molecular changes go with faster aging. This study points to the loss of silencing over ancient viral DNA.
Know this first
Context from the editor, not the article · 27 sec
1 · Big dogs die younger
Across species, bigger animals usually live longer. Within dogs it runs the other way: large breeds live much shorter lives than small breeds, even though they share physiology, diets and homes with their owners.
2 · Epigenetic clocks
DNA methylation means chemical tags on DNA that help control which genes are switched on. The tags at some sites change steadily with age. Statistical models called epigenetic clocks read those sites to estimate biological age.
3 · Transposable elements
Roughly half of a mammal's genome is transposable elements, DNA that can copy itself to new places. Much of it comes from ancient viruses. Cells normally keep it quiet, partly by heavily methylating it.
5/5KFF Health News· Christine Mai-Duc· Oct 16
California's next governor inherits a strained Medicaid program and federal cuts
California widened Medi-Cal, its Medicaid program, until it covered 1 in 3 residents. Federal cuts and borrowed money now leave the next governor choosing between raising taxes, trimming coverage, or both.
Why it matters · California is the largest test of how a generous state Medicaid program handles the 2025 federal cuts. More than 2 million people could lose coverage, and hospitals would absorb the costs.
Know this first
Context from the editor, not the article · 30 sec
1 · How Medicaid is funded
Medicaid is health coverage for low-income and disabled people, paid for jointly. The federal government covers a share of each state's costs. Under the Affordable Care Act it pays 90% for adults who gained coverage through the expansion.
2 · Provider taxes
Many states tax hospitals or health plans and spend the money on Medicaid. Every state dollar draws extra federal matching money, and much of it goes back to providers. The 2025 federal law limits this practice.
3 · The 2025 federal law
Republicans passed the One Big Beautiful Bill Act in 2025. It is expected to cut federal Medicaid spending by more than $900 billion over 10 years, mainly through work requirements for adults under 65 and limits on state financing methods.
Randomly assigning women to treatment or comparison groups means differences in babies can be credited to the therapy. That only holds for the randomized comparison, not for links found later within the sample.
An illustrative photo of an infant at play; the six-month tests measured babies' reactions to unfamiliar toys.
A randomized trial suggests that treating depression during pregnancy with short talk therapy may change how the baby's brain develops. The researchers, led by psychologist Elysia Poggi Davis at the University of Denver, published the work in Nature Communications and describe it in The Conversation.
The trial
The researchers enrolled 234 pregnant women who reported depression symptoms at routine prenatal visits in the first or second trimester. Half were randomly assigned to 1, a version of 2 (a brief talk therapy focused on relationships) adapted for pregnancy. It consists of eight 50-minute sessions on interpersonal skills, reducing conflict and building social support.
The comparison group did not go untreated. These women got education about mental health, coping strategies and referrals to community services. Both groups also kept their usual medical care, which could include therapy or medication.
An earlier paper from the project reported that depression diagnoses fell from 36% before MOMCare to 6% after it. Women in the MOMCare group were also more likely to carry to term. The article does not give the comparison group's figures.
What the scans showed
The babies had 3 scans within a few weeks of birth. In the MOMCare group, the 4, a region involved in learning, memory and regulating emotion, was about 5% smaller by volume.
At six months, the babies faced unfamiliar things in the lab, such as a noisy robot that moved unpredictably. Earlier research ties stronger negative reactions to tasks like this with more depression and anxiety in adolescence. Babies with a smaller hippocampus at birth reacted less negatively.
A smaller brain region sounds like a bad sign, and in adults it often is. The authors argue that infant brains are still growing, and faster growth isn't always better. One hypothesis holds that stress speeds up early brain development, possibly too much.
Caveats
The 5% difference comes from the randomized comparison. The link between hippocampus size and infant reactions is a correlation within the sample, so it doesn't show the therapy caused calmer babies.
The article gives no confidence intervals and doesn't say how many babies were scanned.
The mechanism is unknown. Stress hormones or inflammation linked to depression are possible routes, but untested.
Whether any of this affects children's long-term mental health is still open. The team plans to follow the families through early childhood.
The authors call this the first study to show that treating prenatal depression may affect infant brain development. They also note it fits a small number of trials linking reduced maternal depression to better emotional development in babies.
Up to 1 in 5 women have depression during pregnancy. A new randomized trial suggests that treating it with a short course of talk therapy may do more than help the mother. It may also change how the baby's brain develops before birth. The study appeared in Nature Communications. Three of its authors, Elysia Poggi Davis, Benjamin Hankin and Catherine Demers, summarize it in The Conversation. All three report funding from the US National Institutes of Health.
The problem
Prenatal depression is common and costly. It raises the risk of pregnancy complications such as high blood pressure and preterm birth, and it raises the child's later risk of mental illness. Pregnancy also offers an unusual opening for treatment, because women see doctors more often then than at most other times in their lives. Treating one patient could help two generations.
Showing that benefit is hard. Children of depressed mothers differ in many ways at once, including genes, home environment and stress. Observational studies can't separate the effect of depression from everything that comes with it. The way around this is to randomly assign treatment and see whether the children differ. That is the design here.
What was done
The team enrolled 234 pregnant women who reported depression symptoms during routine prenatal appointments. The women joined in the first or second trimester and were randomly split into two groups.
One group received 1, a form of brief 2 adapted for prenatal depression. Interpersonal psychotherapy is a structured talk therapy that treats depression by working on relationships rather than exploring the past. MOMCare consists of eight 50-minute sessions on interpersonal skills, reducing conflict and strengthening social support.
The other group was an 3, not a no-treatment control. These women received education about mental health, strategies for managing symptoms and referrals to community services such as therapy. Both groups continued their usual medical care, which could include referrals to therapy or medication. This makes the test stricter, because MOMCare is being compared with a reasonable level of support, not with nothing.
In an earlier paper from the same project, the authors reported that 36% of enrolled mothers had a depression diagnosis before MOMCare and 6% after. They also reported that women in the MOMCare group were more likely to carry to term. Full-term birth is linked with shorter hospital stays and better child outcomes, including school performance. The article doesn't give the comparison group's depression rates, so the summary alone doesn't show how much of that drop is due to MOMCare rather than time or the comparison support.
The brain findings
Within a few weeks of birth, the babies had magnetic resonance imaging (4) to measure the volume of different brain regions. The finding the authors highlight concerns the 5, a structure involved in learning, memory and emotional regulation. It was about 5% smaller in infants whose mothers received MOMCare.
At six months, the babies returned to the lab for standard tests of how they respond to unfamiliar experiences. One example was a noisy toy robot that danced and moved unpredictably. Earlier studies have found that babies who react more negatively to tasks like this have higher levels of depression and anxiety in adolescence, so these reactions serve as a rough early marker of later risk.
Babies with a smaller hippocampal volume at birth tended to react less negatively.
Why smaller might not mean worse
In adults, a smaller hippocampus is often associated with harm, including in depression. The authors argue that infancy is different. The brain is growing quickly, and faster growth isn't always an advantage. They point to a hypothesis that stress can accelerate early brain development. On that view, mothers' untreated depression might push the fetal hippocampus to grow faster than ideal, and treatment might bring it back toward a more typical pace.
An analogy, offered only as an illustration: a plant forced into fast growth under stress may get taller sooner but end up less sturdy. On this reading, "bigger, earlier" isn't automatically healthier. The article presents this as a hypothesis, not a demonstrated mechanism.
How strong is the evidence?
The design deserves credit. Randomization, an active comparison group and brain imaging within weeks of birth together make a stronger test than the observational studies that dominate this field. The authors call it the first study to show that treating prenatal depression may affect infant brain development. They place it alongside a small but growing set of randomized trials in which reducing maternal depression improved babies' emotional development and changed stress-related hormones.
There are important limits:
Two kinds of evidence are mixed together. The 5% hippocampal difference is a randomized comparison between groups. The link between smaller volume and calmer six-month reactions is a correlation within the sample. The article doesn't say whether MOMCare babies themselves reacted less negatively, so it doesn't show a causal chain from therapy to brain to behavior.
Missing numbers. The summary gives no confidence intervals, p-values, or count of how many of the 234 infants were scanned and retested. Infant MRI often loses participants to movement, so the analyzed sample may be smaller.
Interpreting direction. Whether a smaller newborn hippocampus is good is an argument from a hypothesis, not an established fact.
Short follow-up. Six-month reactions are an early proxy. Whether they translate into less anxiety or depression in childhood or adolescence is unknown.
"Big difference." The authors describe the gap between groups as big despite the active comparison, but the article doesn't quantify that apart from the 5% figure.
What's still open
The authors say the mechanism is unclear. Stress-related hormones or inflammation associated with depression are plausible ways a mother's mood could affect fetal brain growth, but the study didn't establish either. They plan to follow the families through early childhood and track depression and anxiety to see whether the brain differences matter in the long run.
For now, the practical message doesn't depend on the brain findings. MOMCare is brief, non-drug and relatively low-cost, and the earlier results suggest it reduced maternal depression and preterm birth. The authors argue these findings support wider access to mental health care during pregnancy. If the infant brain results replicate, they would add a biological reason to that case.
Remember
The comparison group got real support, yet the therapy group's babies still differed in hippocampus size.
The link between hippocampus size and calmer infant reactions is a correlation, not a randomized result.
Reading a smaller newborn hippocampus as beneficial depends on an untested hypothesis that stress speeds up brain growth.
A 20-year study of older adults in China asked how much of the longevity advantage of better-off people comes from healthier habits. The answer was about a fifth. Reason, who writes the Fight Aging! blog, highlights the open-access paper and its caveats.
The question
People with higher 1, meaning a mix of education, wealth and occupation, live longer and age in better health. Why is unclear. They may smoke less and exercise more, or they may breathe cleaner air, carry fewer chronic infections and get better medical care. Observational data struggle to tell these apart.
The researchers used 2. This method estimates how much of the link between an exposure (low SES) and an outcome (death) runs through a middle factor (lifestyle). It is only causal if its strong assumptions hold.
The study
The researchers followed 33,541 adults aged 65 or older across 23 Chinese provinces for 20 years. They sorted participants into low, medium and high SES using 3, a method that groups people by patterns across education, finances and occupation. Lifestyle was scored on four things: never smoking, no heavy drinking, regular physical and leisure activity, and a healthy diet. "Unhealthy ageing" covered decline in physical, cognitive, mental, vision and hearing function.
The results
Compared with high-SES participants, low-SES participants had a 25% higher death rate (4 1.25) and a 46% higher rate of 5 (hazard ratio 1.46). These figures were adjusted for other measured factors.
Lifestyle accounted for 20.5% of the mortality gap and 16.4% of the unhealthy-ageing gap.
Healthy habits were linked to longer life in every group, but the gain grew with status. From age 65, the healthiest group lived longer than the least healthy group by:
3.18 years (1.40 of them healthy) in the low-SES group
3.76 years (2.73 healthy) in the medium-SES group
5.65 years (3.90 healthy) in the high-SES group
So on these numbers, better habits alone would not close the gap between classes. They might even widen it.
Caveats
This is an observational study. Reason notes that firm conclusions rarely come from this kind of work. Lifestyle was measured only after age 65, so earlier decades of habits are missed. Frailty can push people into less healthy routines, which would blur cause and effect. Unmeasured confounders could shift the estimates. The study doesn't measure the likely explanations for the other ~80%, such as pollution, infections and access to medical care.
For individuals, healthy habits were still linked to years of extra life. For policy, the findings suggest that campaigns aimed at personal behaviour, on their own, will leave most of the gap in place.
A new open-access paper tries to answer a long-running question in epidemiology: when wealthier, better-educated people live longer, how much of that comes down to how they live? Reason, who writes the Fight Aging! blog, summarises the result. Habits such as smoking, drinking, exercise and diet account for only a modest share of the gap, roughly 16–20%.
The question and why it's hard
Socioeconomic status (SES), meaning a combination of education, income or wealth and occupation, is one of several linked traits that predict longevity. Intelligence and education are others. These traits are tangled together, and it is hard to say which causes which. Reason notes that "concrete proof of any sort of causation is challenging to conjure forth from epidemiological databases." Researchers can't randomise people into poverty. They have to work with observational cohorts, groups of people followed over time, and use statistical tools to tease apart possible pathways.
The tool used here is 1. You have an exposure (low SES), an outcome (death or poor health in old age) and a candidate middle step, the mediator (an unhealthy lifestyle). The method estimates how much of the exposure–outcome link would disappear if the mediator were the same across groups. That share is the "proportion mediated."
A simple illustration, with made-up numbers: suppose low-SES people die at a 25% higher rate than high-SES people. If the analysis estimates that removing lifestyle differences would shrink that excess to about 20%, then lifestyle "mediates" roughly a fifth of the gap. The other four-fifths runs through other pathways or through things the model doesn't capture.
The study
The cohort included 33,541 adults aged 65 or older from 23 provinces in China, followed for 20 years. (The article doesn't name the underlying survey.)
SES was not one measure. Using 2, a statistical method that sorts people into hidden groups based on patterns across several variables, the researchers put participants into low, medium or high SES classes based on education, financial status and occupation.
Healthy lifestyle score gave points for never smoking, no heavy drinking, regular physical and leisure activity, and a healthy diet.
Outcomes were all-cause mortality and "3." Unhealthy ageing was defined across five areas of function: physical, cognitive, mental, vision and hearing.
The results
Compared with high-SES participants, low-SES participants had:
an adjusted 4 of 1.25 for all-cause mortality (about 25% higher death rate after accounting for other measured factors)
an adjusted hazard ratio of 1.46 for unhealthy ageing
Healthy lifestyle mediated 20.5% of the SES gap in mortality and 16.4% of the gap in unhealthy ageing.
The study also compared the healthiest-lifestyle group with the least healthy group inside each SES class, measured from age 65:
Two points stand out. First, a healthy lifestyle was linked to more years of life in every group, including the poorest. Second, the payoff grew with status. High-SES people with the best habits gained about 5.7 extra years, nearly 4 of them healthy. Low-SES people gained about 3.2 years, only 1.4 of them healthy. On these figures, better habits across the board would not close the gap between classes and might even widen it. The article doesn't analyse why. Plausible explanations include better medical care or cleaner environments that let healthy habits pay off more, but these are guesses, not findings.
What else might explain the gap
If lifestyle accounts for a fifth, something else accounts for most of the rest. Reason lists other candidates that differ by SES and have been studied on their own: exposure to air pollution, exposure to persistent infections, and access to medical care. This study doesn't measure any of them, so it can't say how the remaining ~80% divides up.
Caveats
Reason himself warns that "firm conclusions do not tend to emerge from studies of this nature." Specific reasons for caution:
Observational design. Mediation estimates are only causal if there is no unmeasured confounding between SES, lifestyle and outcomes. In a real population, that assumption is almost certainly violated to some degree.
Late-life measurement. Lifestyle was measured at age 65 or older. Decades of earlier smoking, diet or physical work aren't fully captured, so lifelong lifestyle could matter more than the 20% suggests.
Reverse causation. People who are already becoming frail tend to exercise less and change their diets. Part of the "healthy lifestyle" signal may reflect health that was already declining.
A coarse score. Lifestyle was reduced to a few yes/no-style components, presumably self-reported (the abstract doesn't say). A crude measure tends to understate how much a mediator explains.
Generalisability. The cohort is Chinese adults who lived through particular historical conditions. The proportions may differ elsewhere.
What it means
For an individual, the message hasn't changed: across all three SES groups, the healthiest habits were linked to several more years of life after 65. For policy, the study adds to evidence that campaigns aimed at personal behaviour, on their own, will leave most of the social gradient in health untouched. The paper doesn't settle what drives the remaining gap. Its value is in narrowing where to look.
Remember
Low-SES older adults had a 25% higher death rate and a 46% higher rate of unhealthy ageing than high-SES peers.
Healthy habits gave high-SES people 3.9 extra healthy years from age 65, but low-SES people only 1.4.
Lifestyle was measured only after 65, so lifelong habits may matter more than the ~20% suggests.
In 1998, US states settled with big tobacco companies to recover smoking-related healthcare costs. Since then the payments have flowed every year, and part of the money was meant for youth anti-smoking programs.
An age-verification prompt on a phone. Teens have beaten these checks with edited photos, makeup and help from older people.
More than 20 countries have enacted or proposed social media bans for minors, and nearly all of them cite youth mental health as a reason. Australia barred under-16s in December 2025, and the U.K. followed. Platforms are also paying in court: Lightman puts YouTube and Meta's 2026 settlements and payouts at more than US$17 billion, over claims that they designed products to hook children. In The Conversation, Carnegie Mellon digital media researcher Ari Lightman argues that bans probably won't fix the problem.
The health case is real but tangled
Lightman cites a 2026 study that found 14-to-20-year-olds are more than twice as likely to have a mental illness as people that age 50 years ago. Global estimates from 2021 put elevated anxiety symptoms at 20.5% of youth and elevated depression symptoms at 25.2%. Jonathan Haidt's book 1 blames social media for much of this, through lost sleep, social comparison and compulsive use. Lightman points to other causes too: better screening and the isolation of COVID-19. He concludes there isn't clear evidence that social media is the main cause. He also argues it has real benefits that alcohol and tobacco lack. In a Pew survey, 80% of U.S. teens said it keeps them connected to friends.
Bans leak
Australia's early data are about compliance, not health. About 61% of 12-to-15-year-olds still use the platforms, through false IDs, altered appearances or 2 (tools that hide a user's location). The 3, Australia's online-safety regulator, found 7 in 10 children with accounts on restricted platforms were still on them. Children fool face-scanning age checks with edited photos, makeup or a parent standing in. Every verification method also requires collecting sensitive personal data.
Where the money goes
Lightman sees one useful parallel with tobacco. In 2026, states will collect $21.7 billion from the 4 and tobacco taxes, but only 3.4% goes to youth anti-smoking programs. Part of an August 2026 Meta settlement is earmarked for mental health programs, but there is no oversight or reporting on how states spend it.
His alternative
Lightman proposes 5 rules. Minors' accounts would get the strongest privacy settings automatically, would not show up in search, and would face limits on addictive design. He would add digital-literacy teaching, screen-free time, and affordable mental health care for children.
The caveat: this is an opinion essay. The data show bans are widely evaded, but nobody has yet measured whether bans or design rules change teenagers' anxiety or depression.
Governments are moving fast to keep minors off social media. Australia barred under-16s in December 2025, and the U.K. followed with a similar rule. Ari Lightman, who studies digital media at Carnegie Mellon University, counts more than 20 countries with bans enacted or proposed, from Greece to the United Arab Emirates to Canada. Platforms are also paying in court: Lightman writes that since March 2026, YouTube and Meta have settled or paid more than US$17 billion in lawsuits. The suits alleged negligence, platforms designed to hook children, and misleading claims about safety and privacy.
In an essay for The Conversation, Lightman asks whether bans will improve young people's mental health. He doubts it. The headline says "early research suggests" bans aren't the answer, but the early data he cites are about whether bans are obeyed. None of it measures whether teenagers' mental health changed. That distinction matters for reading his argument.
Why bans, and why it's hard to know if they'd work
The bans differ in age cutoffs, parental-consent rules and how ages are checked. Most cover some mix of Snapchat, YouTube, TikTok, Instagram, Facebook and X. Motives also vary. Some governments worry about foreign-owned platforms, and others about children's privacy. Nearly all of them name mental health as a reason.
The mental health concern is real. Lightman cites a 2026 study that found people aged 14 to 20 are more than twice as likely to have a mental illness as people that age 50 years ago. Global estimates from 2021 put elevated anxiety symptoms at 20.5% of young people and elevated depression symptoms at 25.2%. Much of the case against social media rests on Jonathan Haidt's 2024 book 1. Haidt argues that social media disrupts social and brain development through lost sleep, fragmented attention, compulsive use, loneliness, social comparison and perfectionism.
Lightman names other causes that make the trend hard to pin on one thing. Screening has improved and awareness is higher, so more cases are detected. COVID-19 lockdowns also increased isolation. His conclusion is that there isn't clear evidence that time on these platforms is the main cause of young people's mental health problems. The article doesn't go through the research on cause and effect. Readers should know that most of it is observational and that experts disagree about how large the effects are.
The alcohol-and-tobacco analogy, and where it breaks
Supporters of bans compare them to age limits on alcohol and cigarettes. Lightman argues that the comparison fails because social media has real benefits. It connects isolated teenagers with like-minded peers and gives them room for self-expression and civic engagement. In a Pew survey, 80% of U.S. teens said social media helps them keep up with their friends' lives.
He does think the tobacco comparison works in one way: how settlement money gets spent. Under the 2, part of the money was meant for youth smoking prevention. In 2026, states will collect $21.7 billion from tobacco settlement payments and tobacco taxes, but only 3.4% of that goes to those programs. Some of the $17 billion from an August 2026 settlement between Meta and a group of states is earmarked for mental health infrastructure, school and community programs, and public health campaigns. Lightman notes there is no oversight of how states use the funds and no requirement to report whether they improve children's well-being. (The article puts total YouTube and Meta payouts at "more than $17 billion" and also says the Meta–states settlement alone was $17 billion. It doesn't reconcile the two figures.)
What the Australian data show
Enforcement is where the evidence is most concrete. Lightman reports that about 61% of Australian children aged 12 to 15 still use the platforms. Millions of accounts were disabled, but children got back on with false IDs, altered appearances or 3 (virtual private networks, which hide a user's location). The article doesn't say where the 61% figure comes from. The Australian 4's own compliance update gives similar numbers: 7 in 10 children who had accounts on restricted platforms were still on them, and more than 80% of Australian 10-to-15-year-olds still use social media frequently. Australia now wants to raise fines on platforms that don't comply. In the U.K., lawmakers are debating limits on consumer VPN access.
Age checks are a weak point. Australia makes platforms responsible for verifying ages, often with biometric "5" that estimate age from a face. Children have beaten these with photo-editing software, pictures of celebrities, makeup, and older friends or parents who take the test for them. Others just enter a false birth year or use an account a relative has already verified. Lightman also notes that every verification method requires collecting sensitive personal data, which creates its own privacy risk. Some policymakers worry that a full ban could push children toward riskier, less moderated corners of the internet.
What Lightman proposes instead
Lightman argues for 6 standards. Platforms would have to switch on the strongest privacy and security settings for minors automatically. For example, accounts would not show up in search unless a user chose to change that, so strangers couldn't easily find a child. The standards would also limit manipulative design and addictive features such as aggressive recommendation algorithms. He adds several other measures:
teaching digital literacy and online safety;
protecting some screen-free time;
helping parents spot signs of compulsive use, and giving families affordable, easy access to mental health care, which he says most places don't have;
following a United Nations recommendation to ask young people what they get from being online and what makes it hard to stop.
What remains open
This is an opinion essay, not a study. The strongest evidence in it is that teenagers widely get around Australia's ban. Even that doesn't settle the health question. A ban that cuts use by a third might still help some teenagers, or it might hurt the isolated teenagers who rely on online communities. The article has no data either way. Safety-by-default is also offered without evidence that it improves mental health. Both policies, bans and design rules, still need outcome studies that track young people's actual anxiety, depression and sleep before and after the rules take effect.
Remember
About 7 in 10 Australian children with accounts stayed on restricted platforms after the under-16 ban.
Nobody has yet measured whether bans change teen anxiety or depression; the data so far cover only evasion.
Tobacco settlement precedent: only 3.4% of related state revenue funds youth prevention, a warning for social media settlements.
Pet dogs show faster age-related epigenetic change when they are larger, according to a study in Science. The difference is biggest in 1, stretches of mobile DNA mostly left behind by ancient viruses that cells normally keep silenced.
Why dogs
Big dog breeds live much shorter lives than small ones, even though all dogs are one species and pet dogs share homes and environments. That makes dogs a natural experiment in why individuals of the same species age at different rates. Comparing very different species, such as mice and whales, can't answer that question well.
What was measured
Researchers used the 2, a large long-term study of pet dogs. They produced 1,640 3 from 894 dogs. A methylome is a map of 4, the chemical tags that help control which genes are active. From these maps they built 5, models that estimate age from methylation patterns. The clocks were off by a median of just 0.82 years.
The clocks seem to track biology, not just birthdays. Dogs whose epigenetic age ran ahead of their real age were more likely to die. Faster epigenetic aging showed up in larger dogs, in males and, perhaps surprisingly, in younger dogs. The abstract doesn't explain the young-dog finding.
Where the changes happen
The pattern depended on the type of DNA:
6, the on-off switches next to genes, mostly gained methylation with age.
7, non-coding stretches inside genes, and transposable elements mostly lost it.
Sex differences were concentrated on the X chromosome. Size differences were concentrated in transposable elements. In larger dogs, age-related loss of methylation at these elements was 31% stronger than in smaller dogs. The effect appeared across many families of these elements and was strongest in young 8, the elements most likely to still be able to copy themselves.
The interpretation, and its limits
Reason, who writes the longevity blog Fight Aging!, argues this supports a wider theory. In his view, losing methylation lets transposable elements wake up, copy themselves, damage genes and make virus-like particles that fuel the chronic inflammation of old age.
The study shows less than that. It measured demethylation, not whether the elements actually became active, and not inflammation. It is also observational: faster demethylation in big dogs could be a cause of shorter lives, a result of them, or a marker of something else that comes with large size. The abstract doesn't say how much higher the risk of death was. The work is a solid lead, not proof of mechanism.
A study published in Science finds that in pet dogs, the epigenetic marks that change with age shift faster in larger dogs. The biggest size difference shows up in 1, stretches of mobile, mostly virus-derived DNA that cells usually keep switched off. The work used data from the 2, a large long-term study that follows ordinary pet dogs living in their owners' homes. Reason, who writes the longevity blog Fight Aging!, discussed the paper. The summary here draws on his post and the paper's abstract.
Why dogs are a useful test case
Comparing species has turned up traits linked to unusually long lives, such as those of naked mole-rats or bowhead whales. But such comparisons say little about why individuals within one species age at different rates. That variation is the kind that matters for people.
Dogs fill the gap. Body size strongly predicts lifespan, and big breeds live much shorter lives than small ones. Yet all dogs belong to one species, and pet dogs share homes, environments and, to a large extent, physiology. If some molecular process tracks both size and lifespan, it is a good candidate for a real driver of aging rate rather than an accident of species differences.
What the researchers did
The team generated 1,640 3 from 894 dogs. A methylome is a map of 4, the chemical tags on DNA that help control which genes are active. There were more samples than dogs, so some dogs were sampled more than once. The researchers paired these maps with each dog's demographic and genetic information.
From the data they built DNA methylation (DNAm) age predictors, also called 5. These are models that estimate a dog's age from methylation at chosen sites. The clocks were accurate, with a median error of 0.82 years.
Next they checked whether the clocks capture biology or only count years. Dogs whose epigenetic age ran ahead of their actual age had a higher risk of death. Here is an illustrative example (not from the paper): a 6-year-old dog whose methylation looks like that of a typical 8-year-old would fall in the higher-risk group. The abstract does not give the size of the mortality effect.
Three groups showed signs of faster epigenetic aging:
Larger dogs. This fits their shorter lives.
Males.
Younger dogs. The abstract does not explain this result. One plausible reading is that methylation changes fastest early in life, but that is an inference, not something the abstract states.
Where in the genome the changes happen
Age-related methylation changes followed a clear pattern by type of DNA:
6, the control switches just upstream of genes, generally gained methylation with age.
7, the non-coding stretches inside genes, and transposable elements (TEs) mostly lost methylation with age.
Sex differences in aging were concentrated on the X chromosome. Size differences were concentrated in TEs. In larger dogs, age-related demethylation of TEs was 31% stronger than in smaller dogs.
That boost was not limited to one family of TEs. It appeared in LINEs (long interspersed nuclear elements, which can copy themselves), SINEs (short interspersed nuclear elements, which borrow LINE machinery to copy themselves), the older LINE2 family, and DNA transposons. It was strongest in evolutionarily young 8. Young LINE1s matter because they are the elements most likely to still be intact and able to copy themselves.
Reason's interpretation
Reason places the result in a broader argument. When aging wears away the methylation that keeps TEs silent, the elements can become active. Active TEs copy themselves around the genome and can break genes. They also make virus-like particles that trigger the immune system, which adds to the chronic inflammation common in old age. He argues the dog study adds to existing evidence that TE activation, driven by epigenetic change, contributes meaningfully to mammalian aging.
That chain of reasoning makes sense, but the study does not show all of it. The abstract reports demethylation of TEs. It does not report that the TEs became more active, that they copied themselves more, or that big dogs had more inflammation as a result.
Caveats
The data are observational. Faster TE demethylation in large dogs is a correlation. It could cause shorter lives, follow from them, or reflect something else that comes with size, such as growth signalling.
Demethylation is not the same as activity. A loss of methylation makes TE activity possible, but this summary contains no measurements of TE RNA, new insertions or inflammation.
Missing numbers. The abstract gives no hazard ratio for the mortality link and no direct comparison of clock speed between breeds of different sizes.
Translation to humans. Dogs are a good model, but body size relates to lifespan differently across species. How far the size–TE link applies to people is unknown.
What it adds
The result is useful. A large, mostly well-matched population of pets shows a clear size–lifespan gradient, and one molecular measure, loss of TE silencing, follows that gradient more strongly than other genomic regions. The obvious next steps are to measure TE expression and inflammation directly in large and small dogs, and to see whether interventions that slow dog aging also slow TE demethylation.
Remember
In a single species, faster demethylation of transposable elements went along with large size, which also predicts shorter life.
Epigenetic age running ahead of real age predicted death in dogs, so these clocks measure more than elapsed time.
Loss of methylation on transposable elements was measured. Whether the elements then became active or caused inflammation was not.
California votes for a new governor in November. The winner inherits 1, the state's Medicaid program for low-income and disabled people, at a moment when it is already short of money and federal cuts are about to begin.
Signs of strain
In March 2025, Medi-Cal ran out of money to pay doctors and hospitals. The state borrowed $3.4 billion internally to keep paying. It had done this a few times before. The unusual part came next: the loan grew to $4.4 billion, and Gov. Gavin Newsom and lawmakers agreed to repay it over 10 years instead of within the year. The 2 (LAO), the legislature's nonpartisan budget adviser, called the move "unusual." Republicans said it leaves the mess to future governors.
How it got so big
California went well beyond federal requirements. From 2024 it covered every low-income resident regardless of immigration status, and it pays for optional benefits such as physical therapy, hospice care and housing help. LAO figures show enrollment has nearly doubled since 2010 and annual spending has risen from $50 billion to $222 billion, more than 40% of the state budget. The program covers 13.6 million people, about 1 in 3 Californians.
The federal squeeze
The 2025 federal law, the 3, is expected to cut federal Medicaid spending by more than $900 billion over a decade. It does this mainly through 4 for adults under 65 and limits on 5, a method in which states tax hospitals to draw extra federal matching money. Fees for some enrollees start in 2028. UC Berkeley and UCLA researchers estimate more than 2 million Californians under 65 could lose coverage over four years. Already, 730,000 have left the program since June 2025.
California has started cutting back too. It froze enrollment for adult immigrants without legal status and will add monthly premiums next year. Several other cuts were pushed to 2027 in hope that the next governor reverses them. Hospitals say they will absorb the cost of patients who lose coverage. One Los Angeles hospital already treats five times its designed capacity, with emergency patients seen in tents in its parking lot.
The candidates
Republican Steve Hilton wants to narrow eligibility and end coverage for immigrants without legal status. Democrat Xavier Becerra, the favorite, promises to shield Californians from the cuts. Beyond cutting administrative waste, he hasn't said how he would raise the tens of billions of dollars needed to keep the program as it is.
Former Medi-Cal director Jennifer Kent's warning to whoever wins: "all of those right things have fiscal consequences."
California votes for a new governor in November, and the winner takes over a Medicaid program that was already short of money before the federal cuts start. In March 2025, 1 (California's version of Medicaid) ran out of money to pay doctors and hospitals. The state borrowed $3.4 billion from its own internal accounts to keep paying. Short-term internal loans like this had happened a few times before. What was new came a few months later. The loan had grown to $4.4 billion, and Gov. Gavin Newsom and Democratic lawmakers agreed to repay it over 10 years rather than later that year. Republican senators said the move would "paper over" a structural deficit and leave "future governors and legislatures to clean up the mess." The nonpartisan 2 (LAO), the legislature's budget adviser, called it "unusual."
How the program got this big
Congress created Medicaid in 1965 for specific groups: low-income families with children, older people and people with disabilities. States have widened it ever since. The biggest step was the Affordable Care Act's expansion to low-income adults without children. California went much further. From 2024 it covered every low-income resident, whatever their age or immigration status. Coverage for people without legal status is mostly paid for by the state, because federal funds generally cover only their emergency care. California also chose to cover benefits that federal law doesn't require, including physical therapy, hospice care and housing assistance.
The LAO's figures show how much this costs. Since 2010, enrollment has nearly doubled and annual spending has gone from $50 billion to $222 billion. Medi-Cal is now more than 40% of all state spending. It covers about 13.6 million people, or 1 in 3 Californians, and California spends more on Medicaid than New York and Texas combined. Rising health care costs everywhere explain part of the growth. The state's own choices explain the rest.
"There is no population that we have met that we don't want to offer coverage to, and we've never met a benefit that we don't like," said Jennifer Kent, who ran Medi-Cal under Gov. Jerry Brown.
What the federal law changes
Federal Medicaid spending is expected to fall by more than $900 billion over 10 years under the 3. Most of the expected coverage losses come from new 4 for adult enrollees under 65. The law also limits 5. In this method, states tax hospitals or health plans and use the money to draw extra federal matching funds. From 2028, states must charge some enrollees fees for many services. New asset limits also apply. Disability advocates say these limits will block access to home care, which they describe as cheaper and more humane than nursing homes.
The UC Berkeley Labor Center and the UCLA Center for Health Policy Research estimate that more than 2 million Californians under 65 could lose coverage over the next four years because of the state and federal changes combined. At least 730,000 people have already left the program since June 2025. The article doesn't say how many of them lost eligibility and how many dropped out because of paperwork.
California has already started cutting back on its own. It froze enrollment for adult immigrants without legal status, and monthly premiums start next year. Democratic lawmakers persuaded Newsom to push several other cuts to 2027, hoping a new governor might reverse them. State agencies are trying to automate work-requirement checks so that eligible people aren't dropped for missing paperwork.
Who absorbs the losses
Under state law, counties are health care providers of last resort. They say they need funding now for the uninsured patients they expect next year. The latest state budget set aside about $390 million for public and financially distressed hospitals. Martin Luther King Jr. Community Hospital in Los Angeles shows the pressure. It treats five times the patients it was built for, and 80% of them are uninsured or on Medi-Cal. Most emergency patients are now seen in tents in the parking lot. CEO Elaine Batchlor expects that "insured care will turn into 6," with providers covering the cost.
The article also profiles Nelly, 59, from Los Angeles County. She had no insurance for years after leaving work to care for her mother. She signed up for Medi-Cal in an emergency room after waking up unable to see out of her left eye. It now pays for her specialist visits and her transport to them. Her condition may exempt her from work requirements, but paperwork problems at renewal have left her afraid of losing coverage anyway.
The candidates
Neither candidate has put forward a detailed plan. Republican Steve Hilton, a former Fox News commentator, wants to narrow eligibility and end coverage for immigrants without legal status, which he calls "wildly unsustainable." He argues that safety-net programs should be just that, and objects to "40% of Californians" being on the program. His figure is higher than the 1-in-3 share the article reports. Democrat Xavier Becerra, the former U.S. health secretary and the favorite to win, has promised to protect Californians from the federal cuts. He opposes the immigrant enrollment freeze and the new premiums, arguing they will push up taxpayer costs for emergency room care. Apart from promising to cut billions in administrative waste, he hasn't said how he would find the tens of billions of dollars needed just to keep the program as it is. He declined to be interviewed.
Reform or retrenchment
Some people see the crisis as a chance to fix a program they consider broken, with long waits for appointments, low payments to providers and unstable funding. Mark Ghaly, Newsom's former top health official, co-chairs the 29-member 7, set up to modernize the program and keep it sustainable. "We know we can't afford to serve everybody we want to serve in the model that we have today," he said. State Sen. Caroline Menjivar, whose Los Angeles-area district is about half on Medi-Cal, is frustrated with putting "millions and millions into the same system." Conservatives say the program is bloated and full of fraud. The article cites no evidence on fraud either way.
The article leaves the key questions open: how much revenue the state will need, which benefits or groups would be cut first, and whether automating work-requirement checks can actually limit coverage losses. Kent's warning sums up the problem: "all of those right things have fiscal consequences."
Remember
Medi-Cal now takes more than 40% of California's state spending, up from $50 billion in 2010 to $222 billion.
Projected coverage losses come mostly from work requirements and paperwork, not changes to who qualifies.
Lost coverage turns into unpaid hospital and county costs, so it doesn't vanish from public budgets.
