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Postpartum depression descended on Kristina Leos like a heavy fog that separated her from everyone she loved. She could see her newborn baby girl, her two older kids, and her husband, but she felt like a ghost passing through their world. “I was going through the motions, but it was like I was looking down on my family,” she recalls.

Leos, 40, a nurse who lives in Midlothian, Tex., tried several different antidepressants and doses. None helped. She messaged a friend, anxious that she was unfit to be a mother. She even asked if they would take her new baby, Victoria. Although Leos never considered hurting her kids, there were times when she was driving home from work and wondered what it would be like to drive off a bridge. “I just had no fear of dying,” she says. “I didn’t care what happened.”

In December 2023, nine months after Leos gave birth to Victoria, her doctor told her they were running out of options. She was down to serious choices, including infusions of ketamine (a drug that alters the anatomy and activity of brain cells), electroconvulsive therapy, or admission to a psychiatric hospital.

Then Leos remembered seeing something on social media about a new drug specifically for postpartum depression. Unlike older antidepressants such as Prozac, this medication worked on brain chemicals that are particularly affected by pregnancy. She asked her doctor about it, and they decided to give it a try. Leos began the medication on New Year’s Day 2024. Three days later, her world shifted. “I was driving on the highway, and I could literally feel this huge cloud lifting over me,” she says. “And every day I got better and better.” The drug, called zuranolone and approved by the U.S. Food and Drug Administration in 2023, has since relieved depression in thousands of women.

This kind of help is needed desperately. For new mothers, the overall leading cause of death during the first year after childbirth is not bleeding or infection, according to one study encompassing 36 states. What kills more are mental health problems, which account for approximately 23 percent of maternal deaths in the country. These disorders include a lot of cases of postpartum depression. Yet fewer than half of the women who show signs of such illness are diagnosed, and even fewer receive any form of treatment.

Emerging research on the biology of postpartum depression shows that it is not like other severe mood disorders neurologically or biochemically. Rather, it is a result of dramatic changes in hormone levels that come with pregnancy and childbirth. Studies have shown that levels of progesterone and a related hormone, allopregnanolone, rise significantly during pregnancy. Then the levels drop sharply after delivery. Some women are particularly sensitive to this drop, which can disrupt the brain circuitry that regulates mood, leaving them unable to effectively deal with the stresses of motherhood. Zuranolone is designed to offset that drop-off.

Growing knowledge of the neurobiology of postpartum depression is also pointing toward methods for earlier and more reliable detection. Many experts hope that identifying biomarkers that predict which women will develop the condition, as well as the introduction of the new medication, will take the stigma away from the illness and stop both health-care workers and patients from viewing it as a sign of personal weakness or poor parenting. “It is a serious mental illness,” says Kristina Deligiannidis, a reproductive psychiatrist at the Feinstein Institutes for Medical Research at Northwell Health in New York State. “We just want to empower women to seek treatment.”

Challenges do remain. The price tag for the two-week course of zuranolone is nearly $16,000, raising concerns about how insurance coverage and looming Medicaid-eligibility cuts could restrict access, especially because Medicaid covers about 40 percent of births in the U.S., and researchers are still trying to figure out why the pill doesn’t work for everyone. “Not every single person that takes it is going to have a fabulous remission of their symptoms,” says Samantha Meltzer-Brody, a psychiatrist and founder of the perinatal psychiatry program at the University of North Carolina School of Medicine in Chapel Hill. Still, she views the medication as a major milestone. “It can work remarkably well for more than half of people, and it’s rapid-acting,” she says. “That’s a game changer.”

For centuries, medicine has struggled to fully grasp the causes and consequences of postpartum depression. Descriptions go as far back as ancient Greece: physicians wrote about women who showed signs of a depressed mood, and even psychosis, after childbirth. During the Middle Ages, new mothers with depressive symptoms were often believed to be possessed by demons or suffering from an imbalance of bile or other body fluids. Postpartum mood disturbances have also been grouped into vague or broad diagnoses such as melancholia, mania, or neurosis, which did little to help patients.

Even in modern times, such distress is often dismissed as “baby blues”—the mood swings that affect most new moms but typically resolve within a couple of weeks. But postpartum depression is more intense and long-lasting. It can cause profound sadness and despair, disrupting the crucial bond between mother and child, and its consequences can affect multiple generations. Every yea,r approximately 500,000 women in the U.S. experience the condition. Approximately 30 percent of women with postpartum depression continue to experience symptoms one year after giving birth. For some, these problems can persist for as long as 11 years.

Yet postpartum depression is not officially recognized as a standalone illness. It did not appear in the Diagnostic and Statistical Manual of Mental Disorders (DSM), the so-called bible of psychiatry, until 1994. Even then it was listed as a subtype of major depression. In the most recent major edition, DSM-5, released in 2013, it is still subsumed under the “major depression” label, with the added phrase “with peripartum onset.” These additional three words reflect evidence that almost half of women develop symptoms during pregnancy, not just after.

Because postpartum depression has been lumped in with major depression, the two have often been treated the same way. Therapy has relied on traditional antidepressants such as selective serotonin reuptake inhibitors (SSRIs) or serotonin and norepinephrine reuptake inhibitors. This approach is rooted in the idea that depression stems from low levels of chemical messengers such as serotonin and norepinephrine that help to govern mood. These antidepressants aim to boost levels of these messengers in the brain.

Not everyone who takes zuranolone is going to have a fabulous remission. Still, it works well for more than half the people. That’s a game-changer.

But in recent decades, the research community has recognized that focusing only on these chemical imbalances leaves out other factors that may underlie postpartum depression—including genetics, inflammation, hormonal changes, and neuroplasticity, the brain’s ability to adapt and form new connections.

Some scientists suspected that fluctuations in hormones such as estrogen and progesterone—called neurosteroids because they act in the brain—played an important role. Yet when research groups started examining the levels of various hormones and neurosteroids, they did not see consistent differences that explained why some new mothers developed depression, and others did not.

Then, about 17 years ago, Jamie Maguire, a neuroscientist now at Tufts University, stumbled on some unusual behavior in mice that had just given birth, and her observation helped to connect the dots. At the time, Maguire was a postdoctoral fellow at the University of California, Los Angeles, studying an ailment called catamenial epilepsy, in which brain seizures become more frequent or more severe during certain phases of the menstrual cycle. She was interested in how neurosteroids might protect against these seizures. Some neurosteroids have been shown to dampen brain activity by strengthening certain effects of a neurotransmitter called gamma-aminobutyric acid, or GABA. This chemical can inhibit neurons, making them less likely to fire. Maguire genetically engineered mice to have altered receptors for GABA on their neurons, making it hard for them to react to the chemical. Without this “brake” on neural activity, the mice’s brains became hyperexcitable. That extreme state can contribute to seizures.

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More than half of the nation’s 623,218 bridges are showing visible signs of deterioration—and now, researchers from the University of Massachusetts Amherst and MIT’s Department of Mechanical Engineering (MechE) have demonstrated a powerful, cost-effective way to extend their lifespan using 3D printing technology.

This breakthrough comes at a crucial time. According to the American Society of Civil Engineers’ 2025 Report Card, 49.1% of U.S. bridges are in “fair” condition, while 6.8% are rated “poor.” The price tag to repair them? Over $191 billion—and that number keeps rising.

A Nationwide Crisis on Our Roads

“Anytime you drive, you go under or over a corroded bridge,” says Simos Gerasimidis, associate professor of civil and environmental engineering at UMass Amherst and former MIT visiting professor. “They are everywhere… their condition often shows significant deterioration. We know the numbers.”

And the numbers don’t lie:

• 623,218 bridges nationwide
• 49.1% fair condition
• 6.8% poor condition
• $191+ billion in projected repair costs

Traditional repairs are expensive, highly disruptive, and often require long-term lane closures—something cities and transportation departments are eager to avoid.

Cold Spray: A 3D Printing Method Reinventing Bridge Repair

The research team turned to cold spray technology, a specialized form of additive manufacturing that deposits metal at high velocity without melting it. This allows steel to bond to corroded bridge sections in the field, in real time, with no major disassembly required.

How Cold Spray Works

1. Fine powdered steel is loaded into a specialized applicator
2. Heated, compressed gas accelerates the particles to supersonic speed
3. The particles strike the corroded beam surface
4. The impact bonds steel to steel—layer by layer—like a metal 3D printer
5. The technician passes the applicator repeatedly, restoring thickness and strength

Because the steel is never melted, the repair is safer, faster, and more structurally consistent than many conventional welding or replacement methods.

Real-World Proof: A Massachusetts Bridge Gets Reinforced

Last month, engineers performed a proof-of-concept repair on a small corroded section of a bridge in Great Barrington, Massachusetts.

The cold spray method:

• Restored missing material
• Reduced corrosion-related vulnerabilities
• Reinforced structural beams
• Caused minimal traffic disruption
• Delivered results at a fraction of traditional repair costs

This demonstration shows that cold spray has the potential to extend the life of thousands of aging bridges—buying cities time and reducing the financial burden of full replacements.

The Future of Infrastructure Repair

Cold spray 3D printing could transform how we maintain transportation networks:

• Rapid field restoration without removing beams
• Lower repair costs, especially for widespread corrosion
• Safer for workers—no high-heat welding
• Sustainability benefits through structural life extension

• Scalable for nationwide adoption

With more than half of America’s bridges in declining condition, this technology introduces a practical, scalable roadmap for infrastructure resilience.

UMass Amherst and MIT’s work may soon influence state and federal repair strategies—ushering in a new era where 3D printing is deployed directly on aging structures to keep roads safe and open.

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Cold spray metal deposition strengthens a deteriorated steel bridge beam with layered 3D-printed metal. Image for illustration only.

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For some folks, breakfast isn’t the most important meal of the day—it’s the most skipped. From 2015 to 2018, 15% of Americans older than 20 skipped breakfast regularly, according to data from the the Centers for Disease Control.1 Whether it’s because mornings can be annoyingly hectic or because intermittent fasting, which limits the amount of time you can eat each day, is a fairly popular weight-loss tactic, it makes sense that some folks just aren’t taking the time to start each day with a meal.

nd while there is evidence that intermittent fasting may help some people lose weight in the short term, skipping breakfast and intermittent fasting can both have some negative health consequences. This includes creating a stress response in the body, which encourages the release of cortisol, encouraging belly fat accumulation over time. Not eating in the morning can also increase feelings of anxiety due to low blood sugar, and it may increase brain fog, since your brain needs to be “fed”—and until it is, it can’t think clearly. After all, glucose is the brain’s primary fuel.

Skipping breakfast might also have some long-term negative consequences on brain health, according to a study released on November 30, 2024, in the Journal of Neurorestoratology.2 Let’s take a closer look at what they found.  

How Was This Study Conducted?

This study was an observational study, meaning that the researchers simply observed participants without creating specific conditions. For example, for other types of studies, participants would be randomly assigned to a group, with one group instructed to skip breakfast and another group instructed to eat breakfast. 

In this case, participants simply did what they normally do and recorded the timing of their meals so that researchers could compare certain characteristics of breakfast skippers to those who eat breakfast. Researchers considered “breakfast skippers” as those who regularly skip breakfast at least once a week. 

To qualify for this study, participants had to be at least 60 years old, live in Chengdu, Sichuan, China, and be willing to complete a three-year follow-up—the length of the study. People with certain co-morbidities, like severe cardiac disease and infections of the central nervous system, were not qualified to participate. 

While 973 individuals made the cut to participate in the study, only 859 made it the whole three-year study period. Of these, 117 were categorized as habitual breakfast skippers. Because of the mismatch in the number of breakfast skippers to breakfast eaters, researchers formed a sub-analysis, creating a 1-to-1 matchup with breakfast skippers to breakfast eaters based on age, sex, education level, and ApoE genotype. This analysis is called 1:1 propensity score matching (PSM).

At baseline, demographic information, including age, sex, and education level, was collected. Participants’ cognitive function was assessed using a test called the Mini-Mental State Examination, which was repeated every 18 months. The MMSE is a brief quiz that tests a person’s recall of simple facts, like what day it is or where they are. All participants were also tested for the ApoE gene, which, when present, increases one’s risk for Alzheimer’s disease.

Of the 859 participants, 179 also underwent brain magnetic resonance imaging (MRI) scans at each follow-up visit to assess brain volume—because where brains are concerned, size matters. Brain atrophy—a shrinking brain—has been linked to dementia. Of the 179 who had MRIs, 34 were considered breakfast skippers. 

At the final 36-month follow-up visit, all participants also underwent additional blood work to assess biomarkers in the blood that signal neurodegeneration. Neurodegeneration is a loss of brain and nervous system function.

What Did This Study Find?

At baseline, there were no significant differences between breakfast eaters and breakfast skippers regarding cognitive performance, based on the MMSE scores. MMSE scores were still similar at the 18-month follow-up. It wasn’t until the final 36-month follow-up that differences between the breakfast eaters and breakfast skippers started surfacing. Those who habitually skipped breakfast had lower MMSE scores than breakfast eaters. This held true even after adjusting for age, sex, education level, BMI, ApoE carrier status, blood pressure, diabetes, and hyperlipidemia (high cholesterol and blood fats). Results were similar for the PSM group, as well.

Researchers then used a type of regression model to help identify the factors related to cognitive decline over time. They found that lower education levels, obesity, hypertension, and habitual breakfast skipping were associated with cognitive decline over the study period. 

In addition, they found that individuals who regularly skipped breakfast had higher levels of certain neurodegeneration biomarkers compared to those who did not skip breakfast. This held true in the PSM group as well. 

Falling in line with these results, the 34 breakfast skippers who underwent MRIs also showed more significant brain atrophy (shrinking) compared to those who ate breakfast. 

How Does This Apply to Real Life?

Because other influencing factors—like age and BMI—were adjusted for, this study suggests that regularly skipping breakfast may be an independent risk factor for cognitive decline in older adults. These researchers feel that habitually skipping breakfast may directly increase certain biomarkers of cognitive decline and reduce brain size. 

One key here is “habitual.” Habits are formed over time, which means that the participants who were skipping breakfast most likely had been doing so well before the study period. And we know that changes to the brain that result in Alzheimer’s disease and other forms of dementia can begin decades before symptoms show up. This means that now is the time to form the habit of eating breakfast if you tend to skip it.

If you are a regular breakfast skipper, examine why. Are you not hungry in the morning? Do you feel like you don’t have time for breakfast? Or did you somewhere along the line just fall into this habit? 

Breakfast doesn’t have to be a huge meal, nor does it have to take a lot of time in the morning. For example, smoothies come together quickly and can be taken with you to work or school. Overnight oats and chia pudding can be meal-prepped so that you have grab-and-go options that are available throughout the week. Ditto for baked oatmeal, egg bites, and muffins. And rotating through a few of those options can keep you from getting stuck in a breakfast rut.

If you’re someone who feels that eating breakfast makes you hungrier mid-morning, it may be because you’re not including enough fiber or protein with your first meal of the day. For example, many boxed cereals don’t have enough of either nutrient to sustain you for long. If cereal is your thing, make sure it’s lower in sugar and higher in fiber. Eat it with cow’s milk, soy milk, yogurt, or kefir for added protein. The fiber-protein combo will help prevent a sudden blood sugar crash, which may leave you with that “hangry” feeling. 

Whole-grain toast with eggs, avocado or a slather of nut butter are other great fiber-protein combo options. 

And who says breakfast has to be confined to what is considered traditional breakfast foods? Last night’s leftovers work, too. 

The Bottom Line

This study suggests that regularly skipping breakfast is linked with cognitive decline in older adults. Because negative changes in the brain can begin decades before symptoms show up, it’s important to start healthier habits now. This includes regularly eating breakfast if you’re not already—even if it’s just something small to feed your brain and break that overnight fast. If you’re in need of ideas, try shuffling through some of our simple, cozy winter breakfast recipes.

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Credit: Getty Images. EatingWell design.

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The U.S. is in the grips of a botulism outbreak tied to a premium infant formula brand. Dozens of babies have been affected as of November 19.

All the reported cases of the paralyzing bacterial infection occurred between August and November and have been linked to powdered infant formula produced by ByHeart, according to a Food and Drug Administration report. The company voluntarily recalled all its products on November 11, and experts caution that more cases of the potentially fatal disease may surface.

“In some cases, after exposure, it may have taken up to a month for some babies to actually show symptoms,” says Randal De Souza, a pediatric infectious disease specialist at Golisano Children’s Hospital at the University of Kentucky.

As of November 19, the FDA and the Centers for Disease and Control and Prevention are currently investigating illnesses in babies from several states, including Arizona, California, Idaho, Illinois, Kentucky, Maine, Michigan, Minnesota, New Jersey, North Carolina, Oregon, Pennsylvania, Rhode Island, Texas, and Washington State.

In an e-mail to Scientific American, ByHeart’s co-founder and president, Mia Funt, said the company was working with the FDA and independent experts on its product recall and ongoing investigations.

“Our number one priority is infant health. We express our deepest sympathy to the families currently impacted by the cases of infant botulism,” Funt wrote. The FDA did not immediately respond to a request for comment from Scientific American.

Here’s what to know about the outbreak and how to stay safe.

What to know about the botulism outbreak in babies

Botulism is a relatively rare but potentially severe infection caused by the soil-dwelling bacterium Clostridium botulinum. The bacterium produces toxins that damage nerves, De Souza says. According to the most recent CDC data, there were 243 lab-confirmed cases in the U.S. in 2021, and 181 of those infections were in infants. Between 5 and 10 percent of cases are fatal.

In infants, the first signs of infection are usually constipation, followed by varying degrees of paralysis. Babies might initially lose control of their facial expressions, mouth, and eyes. They might also drool more, take longer to feed or have a weaker cry, De Souza says. The paralysis slowly progresses down through the body, he explains.

“The presentation tends to be a ‘floppy baby,’ which essentially means you lose head control first, then you lose limb control, and the last tends to be respiration: you lose your ability to breathe,” De Souza says.

How are infected infants diagnosed and treated?

A clinical diagnosis, using stool samples, can take up to a week, so any infant with a suspected case of botulism must be monitored closely, De Souza says.

If infants are hospitalized, they are placed on feeding tubes and may be intubated. Infections are treated with an antitoxin that binds to and neutralizes excess toxins in the body to stop the infection.

“Then it’s up to the body to essentially regenerate nerves,” De Souza says. That process can take weeks or months, and some babies may require further speech or feeding therapy. In extreme cases, they might require a breathing tube.

Infants who recover from botulism aren’t known to have permanent issues, De Souza says, but “a very young baby requiring multiple support modalities for months is not great.”

All 23 infants that were infected in the recent outbreak—almost all of whom are currently under seven months old—have been hospitalized, and no deaths have been reported.

How to stay safe

ByHeart and the FDA are alerting people not to use recently purchased ByHeart infant formula. Barbara Kowalcyk, director of the Institute for Food Safety and Nutrition Security at George Washington University, says to check any ByHeart formula parents might have stocked up.

“People have stuff in their pantries that they don’t always know about, or they may not hear about the recall,” Kowalcyk says. “The voluntary recall language can lead people to potentially believe that it’s not as big of an issue.”

She suspects that more cases of botulism will be uncovered in the coming weeks.

Is baby formula particularly susceptible to botulism?

Botulism has been detected in baby formula before. The pathogen mostly exists as a hardy spore, and while high pressure or heat at an industry level can kill them, “your typical heating, say, in your home kitchen will not,” De Souza says. Otherwise, “the spores just live forever.”

According to the Infant Botulism Treatment and Prevention Program (IBTPP), 84 infants in the U.S. have received treatment for botulism since August, and at least 36 of those cases have been linked to powdered infant formula exposure. The California Department of Public Health found at least six cases of infant botulism linked to exposure to ByHeart powdered formula that occurred from November, 2024 to June, 2025—months before the current outbreak.

It’s unclear if C. botulinum contamination occurred at any point during the manufacturing process at ByHeart’s facilities or at stores that sold the product, or in people’s homes after that process. The California Department of Public Health reported on November 8 that an already opened can of ByHeart formula tested positive for C. botulinum, and officials are now testing unopened products for the bacterium.

In an open letter to the FDA, ByHeart alluded to a wider “unprecedented spike” in national infant botulism. Representatives of IBTPP have also said that the spike in cases may be indicative of a broader trend, the Associated Press reported.

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Natalie Johnston was scrolling on Facebook a couple of years ago, when she came across a group called, “One And Done On The Fence”. Seeing it, she felt a sense of relief.

“It was nice to hear someone giving it a name,” she says.

She and her husband have a five-year-old daughter called Joanie, but they knew they probably wouldn’t have a second child, not because they couldn’t, but not out of choice, either: Natalie finds it hard to imagine having the time and money for one.

“You know you’d love that baby, everyone tells you, but there’s a little teeny niggle where you think, ‘what if I put my first in that position where she can’t do the activity she wants to do because I’ve got to spread money out between two’?”

She adds: “Is it okay to say you’re only having one because they don’t fit into modern ways of parenting?”

Modern parenting, for Natalie, 35, looks like family holidays with Joanie. It looks like weekday evenings hearing about her day at school and helping her with homework. But, with demanding jobs and no family living nearby to help with childcare, it also looks like an expensive childcare jigsaw.

But ultimately, deciding whether or not to have a second is a tough decision. “I think you worry you’d regret it,” she says.

The fertility rate was 1.41 children per woman in England and Wales last year, according to the Office for National Statistics (ONS) – the lowest on record for a third year running.

And the proportion of families with one child has grown since the turn of the century.

They made up 44% of all families with dependent children in England and Wales last year, up from 42% in 2000. (Though the peak was 47% in the early 2010s, which then dipped before picking up again after Covid.)

The UK’s falling birth rate is part of what the United Nations calls a “global fertility slump”, which it puts down, in part, to money worries.

People aren’t “turning their backs on parenthood”, says the UN in a summary of its Population Fund’s State of World Population report, which surveyed people across 14 countries.

Instead, it says they “are being denied the freedom to start families due to skyrocketing living costs, persistent gender inequality and deepening uncertainty about the future”.

Bridging the ‘fertility gap’

Education Secretary Bridget Phillipson said earlier this year that she wants “more young people to have children, if they so choose”.

She pointed to the expansion of funded childcare hours in England as a way the government was trying to recover “dashed dreams”.

Annual nursery costs for a child under two in England did fall this year for the first time in 15 years, according to the children’s charity Coram. They are now an average of £12,425, down 22% on the previous year. However, they are slightly up in Scotland and Wales, at £12,468 and £15,038 respectively.

A study from University College London (UCL) last year suggested two-fifths of 32-year-olds in England want children – or more children, if they are already parents – but only one in four of them are actively trying to conceive.

Dr Paula Sheppard, an anthropologist at the University of Oxford, believes parents in the West still think of having two children as “the norm”.

However, she says there is a “fertility gap” and that “for every three kids wanted… only two are born”.

“A lot of this gap is driven by… people starting families later and later in life,” she explains – often a result of education and career opportunities for women and changing gender roles.

“It becomes a whole lot more difficult to get pregnant [and] it becomes a whole lot more difficult to keep the pregnancy.”

Fewer pupils, less cash for schools

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Bridging the ‘fertility gap.’

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Before we go any further, it’s important to define our terms. This newsletter is going to focus on the laws of war, not a related concept called rules of engagement. The laws of war reflect the mandatory, minimum level of lawful conduct, and all soldiers are legally obligated to obey them at all times and in all conflicts.

Rules of engagement are rules devised by commanders that are often more restrictive than the laws of war. For example, when I was in Iraq, our rules of engagement sometimes kept us from attacking lawful targets, in part because we wanted to be particularly careful not to inflict civilian casualties.

In my service, we were often frustrated by the rules of engagement. We did not, however, question the laws of war.

There are now good reasons to believe that the U.S. military, under the command of President Trump and Hegseth, his secretary of defense, has blatantly violated the laws of war. On Nov. 28, The Washington Post reported that Hegseth issued a verbal order to “kill everybody” the day that the United States launched its military campaign against suspected drug traffickers.

According to The Post, the first strike on the targeted speedboat left two people alive in the water. The commander of the operation then ordered a second strike to kill the shipwrecked survivors, apparently — according to The Post — “because they could theoretically call other traffickers to retrieve them and their cargo.” If that reporting is correct, then we have clear evidence of unequivocal war crimes — a no quarter order and a strike on the incapacitated crew of a burning boat.

And if it’s true, those war crimes are the fault not of hotheaded recruits who are fighting for their lives in the terrifying fog and fury of ground combat but rather of two of the highest-ranking people in the American government, Hegseth and Adm. Frank M. Bradley, the head of Special Operations Command — the man the administration has identified as the person who gave the order for the second strike.

My colleagues in the newsroom followed on Monday with a report of their own, one that largely mirrored The Post’s reporting, though it presented more evidence of Hegseth’s and Bradley’s potential defenses. Hegseth, our sources said, did not order the second strike, and the second strike might have been designed to sink the boat, not kill survivors.

But if that’s the explanation, why wasn’t the full video released? The administration released limited video footage of the first strike, which created the impression of the instant, total destruction of the boat and its inhabitants. Now we know there was much more to see.

At the same time, Hegseth and the Pentagon have offered a series of puzzling and contradictory statements. Sean Parnell, the Pentagon spokesman, told The Post that its “entire narrative was false.”

Hegseth weighed in with a classic version of what you might call a nondenial denial. In a social media post, he said the Post report was “fabricated, inflammatory, and derogatory,” but rather than explain what actually happened (and make no mistake, he knows exactly what happened), he followed up with an extraordinary paragraph:

As we’ve said from the beginning, and in every statement, these highly effective strikes are specifically intended to be “lethal, kinetic strikes.” The declared intent is to stop lethal drugs, destroy narco-boats, and kill the narco-terrorists who are poisoning the American people. Every trafficker we kill is affiliated with a Designated Terrorist Organization.

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Illustration by George Douglas; source photographs by Douglas Sacha and SENEZ/Getty Images

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