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Trump blames Tylenol for autism, dismaying experts

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Trump blames Tylenol for autism, dismaying experts

President Trump blamed the over-the-counter drug acetaminophen, commonly known by the brand name Tylenol, as a significant factor in the rise of U.S. autism diagnoses on Monday, at a news conference in which he offered often inaccurate medical advice for the nation’s children and pregnant women.

“Taking Tylenol is not good. I’ll say it. It’s not good,” Trump said, flanked by Health and Human Services Secretary Robert F. Kennedy Jr. and Centers for Medicare & Medicaid Services Administrator Dr. Mehmet Oz.

In a series of rambling, error-filled remarks that touched upon pain relievers, pregnancy, vaccines and the Amish — who he inaccurately said have no autism prevalence in their communities — Trump also said that the mumps, measles and rubella vaccine should be broken up into multiple shots and that children defer until age 12 the hepatitis B vaccine series now started at birth.

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“I’m just making these statements from me, I’m not making them from these doctors,” he said. “It’s too much liquid. Too many different things are going into that baby.”

The announcement was met with dismay from autism researchers and advocates who said that research thus far into causal links between acetaminophen and autism has turned up minimal evidence.

“Researchers have been studying the possible connections between acetaminophen and autism for more than a decade,” said Dr. David Mandell, a professor of psychiatry at the University of Pennsylvania Perelman School of Medicine. The Trump administration, he said, “has cherry-picked findings that are not in line with most of the research.”

Physicians and researchers also took issue with Trump’s insistence that there was “no downside” to women avoiding fever-reducing drugs in pregnancy. In fact, studies show that untreated fever in pregnancy is associated with higher risk of heart and facial birth defects, miscarriage and neurodevelopmental disorders — including autism.

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The U.S. Food and Drug Administration will initiate a safety-label update for Tylenol and other acetaminophen products and send a letter to physicians about potential links between the drug’s use and autism, Kennedy said.

The actual text of the letter is much milder than Trump’s impassioned critique.

“In the spirit of patient safety and prudent medicine, clinicians should consider minimizing the use of acetaminophen during pregnancy for routine low-grade fevers. This consideration should also be balanced with the fact that acetaminophen is the safest over-the-counter alternative in pregnancy among all analgesics and antipyretics,” states the letter, signed by FDA Commissioner Dr. Marty Makary.

Monday’s announcement followed weeks of speculation that Kennedy planned to publicly link Tylenol usage to autism, which prompted multiple medical associations to release statements clarifying that any evidence of a causal relationship between the two is limited, and that the drug is safe to take during pregnancy with medical advice.

“All of us in the advocacy community, and all of us who have children with autism, had very high hopes that RFK and the President were serious when they said they wanted to find the causes of autism,” said Alison Singer, co-founder and president of the Autism Science Foundation. “The problem is that so far, what we’ve heard has not been gold-standard science.”

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The administration also said it would fast-track the labeling of leucovorin, a generic drug currently used to reduce side effects of chemotherapy, as a treatment for autism-related speech deficits. Also known as folinic acid, leucovorin is a form of the B vitamin folate. Research into its effect on autistic children is still in its early stages, researchers said. The few studies that have been published had small sample sizes and found only minimal improvements in symptoms of concern, Mandell said.

“I want to see a large, rigorous, independent trial. In the absence of that, to tout this as a cure is reckless,” he said. “Families deserve better.”

Autism spectrum disorder is a complex neurological and developmental condition. Symptoms cluster around difficulties in communication, social interaction and sensory processing, and the condition can manifest in many different ways based on co-occurring disabilities and other factors.

Diagnoses in the U.S. have risen steadily since the Centers for Disease Control and Prevention began tracking data in 2000, thanks in large part to a broadening definition of the disorder and increased efforts to identify children with ASD.

Today one in 31 U.S. 8-year-olds has been identified as having autism spectrum disorder, according to the most recent CDC data, up from one in 150 in 2000.

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Kennedy has long asserted that’s due to an external environmental cause, often using inaccurate statements to describe both the condition and the research around it.

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Most experts believe genetic links and changing diagnostic criteria play a significant role in the trend. In April, Kennedy dismissed such research and arguments as “epidemic denial.” He said he was certain an external factor was to blame.

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“We know it’s an environmental exposure. It has to be,” Kennedy said. “Genes do not cause epidemics.” He said at the time that the administration would find an environmental cause by September.

Research into causal links between acetaminophen and autism have not found strong evidence.

Last year, a team of researchers from the U.S. and Europe reviewed records of 2.5 million babies born in Sweden between 1995 and 2019. At first glance, it did seem like children exposed to acetaminophen in the womb were 5% to 7% more likely to be diagnosed with autism than those who weren’t. But when the researchers compared those children to their siblings, they found that kids from the same parents were equally likely to be diagnosed with autism, whether their mother took acetaminophen during pregnancy or not.

“If you actually do an apples to apples comparison, you see absolutely zero effect. The association flatlines. In other words, there’s no real risk that’s attributable to acetaminophen,” said Brian K. Lee, a professor of epidemiology and biostatistics at Drexel University who was on the study team. “A large elephant in the room is being ignored, and that’s genetics.” Hundreds of studies over the years have explored the complex genetics of autism, with both inherited and spontaneous genes contributing to the condition.

The paper also noted that women who took acetaminophen while pregnant were, unsurprisingly, more likely to suffer from the kinds of ailments for which the medication is indicated, like fevers or chronic pain.

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They were also more likely to have diagnoses of autism or other neurodevelopmental disorders, to have pre-existing mental health conditions or to be taking other prescribed medications, the team found. Their results were published in the Journal of the American Medical Association.

“People don’t take acetaminophen for fun. They are taking it for a health condition,” Lee said.

He compared the correlation between Tylenol exposure and autism to the correlation between ice cream sales and drownings. Both of those things tend to increase at the same time each year, he said, not because ice cream is deadly but because both rise during hot summer months. In other words, the underlying health causes that women are taking acetaminophen to treat could be more likely linked to autism than the pain reliever itself.

“This is just such a shame when there are so many things we could do to help autistic children and adults, and the negative consequences — making parents feel guilty about taking Tylenol during pregnancy and newly pregnant women afraid — are real,” said Catherine Lord, a clinical psychologist and autism researcher at UCLA. “Just sad all around.”

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Contributor: Is there a duty to save wild animals from natural suffering?

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Contributor: Is there a duty to save wild animals from natural suffering?

The internet occasionally erupts in horror at disturbing images of wildlife: deer with freakish black bubbles all over their faces and bodies, sore-ridden squirrels, horn-growing rabbits.

As a society, we tend to hold romanticized notions about life in the wild. We picture these rabbits nuzzling with their babies, these squirrels munching on some nuts and these deer frolicking through sunlit meadows. Yet the trend of Frankenstein creatures afflicted with various diseases is steadily peeling back this idyllic veneer, revealing the harsher realities that underpin the natural world. And we should do something about it.

First, consider that wild animals — the many trillions of them — aren’t so different from other animals we care about — like dogs and cats — or even from us. They love. They build complex social structures. They have emotions. And most important, they too experience suffering.

Many wild animals are suffering because of us. We destroy their habitats, they’re sterilized and killed by our pollution, and sometimes we hunt them down as trophies. Suffering created by humans is especially galling.

But even in the absence of human impact, wild animals still experience a great deal of pain. They starve and thirst. They get infected by parasites and diseases. They’re ripped apart by other animals. Some of us have bought into the naturalistic fallacy that interfering with nature is wrong. But suffering is suffering wherever it occurs, and we should do something about it when we can. If we have the opportunity to rescue an injured or ill animal, why wouldn’t we? If we can alleviate a being’s suffering, shouldn’t we?

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If we accept that we do have an obligation to help wild animals, where should we start? Of course, if we have an obvious opportunity to help an animal, like a bird with a broken wing, we ought to step in, maybe take it to a wildlife rescue center if there are any nearby. We can use fewer toxic products and reduce our overall waste to minimize harmful pollution, keep fresh water outside on hot summer days, reduce our carbon footprint to prevent climate-change-induced fires, build shelter for wildlife such as bats and bees, and more. Even something as simple as cleaning bird feeders can help reduce rates of disease in wild animals.

And when we do interfere in nature in ways that affect wild animals, we should do so compassionately. For example, in my hometown of Staten Island, in an effort to combat the overpopulation of deer (due to their negative impact on humans), officials deployed a mass vasectomy program, rather than culling. And it worked. Why wouldn’t we opt for a strategy that doesn’t require us to put hundreds of innocent animals to death?

But nature is indifferent to suffering, and even if we do these worthy things, trillions will still suffer because the scale of the problem is so large — literally worldwide. It’s worth looking into the high-level changes we can make to reduce animal suffering. Perhaps we can invest in the development and dissemination of cell-cultivated meat — meat made from cells rather than slaughtered animals — to reduce the amount of predation in the wild. Gene-drive technology might be able to make wildlife less likely to spread diseases such as the one afflicting the rabbits, or malaria. More research is needed to understand the world around us and our effect on it, but the most ethical thing to do is to work toward helping wild animals in a systemic way.

The Franken-animals that go viral online may have captured our attention because they look like something from hell, but their story is a reminder that the suffering of wild animals is real — and it is everywhere. These diseases are just a few of the countless causes of pain in the lives of trillions of sentient beings, many of which we could help alleviate if we chose to. Helping wild animals is not only a moral opportunity, it is a responsibility, and it starts with seeing their suffering as something we can — and must — address.

Brian Kateman is co-founder of the Reducetarian Foundation, a nonprofit organization dedicated to reducing consumption of animal products. His latest book and documentary is “Meat Me Halfway.”

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Ideas expressed in the piece

  • Wild animals experience genuine suffering comparable to that of domesticated animals and humans, including through starvation, disease, parasitism, and predation, and society romanticizes wildlife in ways that obscure these harsh realities[1][2]
  • Humans have a moral obligation to address wild animal suffering wherever possible, as suffering is morally significant regardless of whether it occurs naturally or results from human action[2]
  • Direct intervention in individual cases is warranted, such as rescuing injured animals or providing fresh water during heat waves, alongside broader systemic approaches like reducing pollution and carbon emissions[2]
  • Humane wildlife management strategies should be prioritized over lethal approaches when addressing human-wildlife conflicts, as demonstrated by vasectomy programs that manage overpopulation without mass culling[2]
  • Large-scale technological solutions, including cell-cultivated meat to reduce predation and gene-drive technology to control disease transmission, should be pursued and researched to systematically reduce wild animal suffering at scale[2]
  • The naturalistic fallacy—the belief that natural processes should never be interfered with—is fundamentally flawed when weighed against the moral imperative to alleviate suffering[2]

Different views on the topic

The search results provided do not contain explicit opposing viewpoints to the author’s argument regarding a moral duty to intervene in wild animal suffering. The available sources focus primarily on the author’s work on reducing farmed animal consumption through reducetarianism and factory farming advocacy[1][3][4], rather than perspectives that directly challenge the premise that humans should work to alleviate wild animal suffering through technological or ecological intervention.

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Contributor: Factory farming of fish is brewing pathogens

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Contributor: Factory farming of fish is brewing pathogens

The federal government recently released new dietary guidelines aimed at “ending the war on protein” and steering Americans toward “real foods” — those with few ingredients and no additives. Seafood plays a starring role. But the fish that health advocates envision appearing on our plates probably won’t be caught in the crystal blue waters we’d like to imagine.

Over the past few decades, the seafood industry has completely revolutionized how it feeds the world. As many wild fish populations have plummeted, hunted to oblivion by commercial fleets, fish farming has become all the rage, and captive-breeding facilities have continually expanded to satiate humanity’s ravenous appetite. Today, the aquaculture sector is a $300-billion juggernaut, accounting for nearly 60% of aquatic animal products used for direct human consumption.

Proponents of aquaculture argue that it helps feed a growing human population, reduces pressure on wild fish populations, lowers costs for consumers and creates new jobs on land. Much of that may be correct. But there is a hidden crisis brewing beneath the surface: Many aquaculture facilities are breeding grounds for pathogens. They’re also a blind spot for public health authorities.

On dry land, factory farming of cows, pigs and chickens is widely reviled, and for good reason: The unsanitary and inhumane conditions inside these facilities contribute to outbreaks of disease, including some that can leap from animals to humans. In many countries, aquaculture facilities aren’t all that different. Most are situated in marine and coastal areas, where fish can be exposed to a sinister brew of human sewage, industrial waste and agricultural runoff. Fish are kept in close quarters — imagine hundreds of adult salmon stuffed into a backyard swimming pool — and inbreeding compromises immune strength. Thus, when one fish invariably falls ill, pathogens spread far and wide throughout the brood — and potentially to people.

Right now, there are only a handful of known pathogens — mostly bacteria, rather than viruses — that can jump from aquatic species to humans. Every year, these pathogens contribute to the 260,000 illnesses in the United States from contaminated fish; fortunately, these fish-borne illnesses aren’t particularly transmissible between people. It’s far more likely that the next pandemic will come from a bat or chicken than a rainbow trout. But that doesn’t put me at ease. The ocean is a vast, poorly understood and largely unmonitored reservoir of microbial species, most of which remain unknown to science. In the last 15 years, infectious diseases — including ones that we’ve known about for decades such as Ebola and Zika — have routinely caught humanity by surprise. We shouldn’t write off the risks of marine microbes too quickly.

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My most immediate concern, the one that really makes me sweat, is the emergence of drug-resistant bacteria among farmed fish. Aquaculturists are well aware that their fish often live in a festering cesspool, and so many growers will mix antibiotics — including ones that the World Health Organization considers medically important for people — into fish feed, or dump them straight into water, to avoid the consequences of crowded conditions and prevent rampant illness. It would be more appropriate to use antibiotics in animals only when they are sick.

Because of this overuse for prevention purposes, more antibiotics are used in seafood raised by aquaculture than are used in humans or for other farmed animals per kilogram. Many of these molecules will end up settling in the water or nearby sediment, where they can linger for weeks. In turn, the 1 million individual bacteria found in every drop of seawater will be put to the evolutionary test, and the most antibiotic-resistant will endure.

Numerous researchers have found that drug-resistant strains of bacteria are alarmingly common in the water surrounding aquaculture facilities. In one study, evidence of antibiotic resistance was found in over 80% of species of bacteria isolated from shrimp sold in multiple countries by multiple brands.

Many drug-resistant strains in aquatic animals won’t be capable of infecting humans, but their genes still pose a threat through a process known as horizontal transfer. Bacteria are genetic hoarders. They collect DNA from their environment and store it away in their own genome. Sometimes, they’ll participate in swap meets, trading genes with other bacteria to expand their collections. Beginning in 1991, for example, a wave of cholera infected nearly a million people across Latin America, exacerbated by a strain that may have picked up drug-resistant adaptations while circulating through shrimp farms in Ecuador.

Today, drug-resistant bacteria kill over a million people every year, more than HIV/AIDS. I’ve seen this with my own eyes as a practicing tuberculosis doctor. I am deeply fearful of a future in which the global supply of fish — a major protein source for billions of people — also becomes a source of untreatable salmonella, campylobacter and vibrio. We need safer seafood, and the solutions are already at our fingertips.

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Governments need to lead by cracking down on indiscriminate antibiotic use. It is estimated that 70% of all antibiotics used globally are given to farm animals, and usage could increase by nearly 30% over the next 15 years. Regulation to promote prudent use of antibiotics in animals, however, has proven effective in Europe, and sales of veterinary antibiotics decreased by more than 50% across 25 European countries from 2011 to 2022. In the United States, the use of medically important antibiotics in food animals — including aquatic ones — is already tightly regulated. Most seafood eaten in the U.S., however, is imported and therefore beyond the reach of these rules. Indeed, antibiotic-resistance genes have already been identified in seafood imported into the United States. Addressing this threat should be an area of shared interest between traditional public health voices and the “Make America Healthy Again” movement, which has expressed serious concerns about the health effects of toxins.

Public health institutions also need to build stronger surveillance infrastructure — for both disease and antibiotic use — in potential hotspots. Surveillance is the backbone of public health, because good decision-making is impossible without good data. Unfortunately, many countries — including resource-rich countries — don’t robustly track outbreaks of antibiotic-resistant pathogens in farmed animals, nor do they share data on antibiotic use in farmed animals. By developing early warning systems for detecting antibiotic resistance in aquatic environments, rapid response efforts involving ecologists, veterinarians and epidemiologists can be mobilized as threats arise to avert public health disasters.

Meanwhile, the aquaculture industry should continue to innovate. Genetic technologies and new vaccines can help prevent rampant infections, while also improving growth efficiency that could allow for more humane conditions.

For consumers, the best way to stay healthy is simple: Seek out antibiotic-free seafood at the supermarket, and cook your fish (sorry, sushi lovers).

There’s no doubt that aquaculture is critical for feeding a hungry planet. But it must be done responsibly.

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Neil M. Vora is a practicing physician and the executive director of the Preventing Pandemics at the Source Coalition.

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A SoCal beetle that poses as an ant may have answered a key question about evolution

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A SoCal beetle that poses as an ant may have answered a key question about evolution

The showrunner of the Angeles National Forest isn’t a 500-pound black bear or a stealthy mountain lion.

It’s a small ant.

The velvety tree ant forms a millions-strong “social insect carpet that spans the mountains,” said Joseph Parker, a biology professor and director of the Center for Evolutionary Science at Caltech. Its massive colonies influence how fast plants grow and the size of other species’ populations. That much, scientists have known.

Now Parker, whose lab has spent 8 years studying the red-and-black ants, believes they’ve uncovered something that helps answer a key question about evolution.

In a paper published in the journal “Cell,” they break down the remarkable ability of one species of rove beetle to live among the typically combative ants.

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The beetle, Sceptobius lativentris, even smaller than the ant, turns off its own pheromones to go stealth. Then the beetle seeks out an ant — climbing on top of it, clasping its antennae in its jaws and scooping up its pheromones with brush-like legs. It smears the ants’ pheromones, or cuticular hydrocarbons, on itself as a sort of mask.

Ants recognize their nest-mates by these chemicals. So when one comes up to a beetle wearing its own chemical suit, so to speak, it accepts it. Ants even feed the beetles mouth-to-mouth, and the beetles munch on their adopted colony’s eggs and larvae.

However, there’s a hitch. The cuticular hydrocarbons have another function: they form a waxy barrier that prevents the beetle from drying out. Once the beetle turns its own pheromones off, it can’t turn them back on. That means if it’s separated from the ants it parasitizes, it’s a goner. It needs them to keep from desiccating.

“So the kind of behavior and cell biology that’s required to integrate the beetle into the nest is the very thing that stops it ever leaving the colony,” Parker said, describing it as a “Catch-22.”

The finding has implications outside the insect kingdom. It provides a basis for “entrenchment,” Parker said. In other words, once an intimate symbiotic relationship forms — in which at least one organism depends on another for survival — it’s locked in. There’s no going back.

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Scientists knew that Sceptobius beetles lived among velvety tree ants, but they weren’t sure exactly how they were able to pull it off.

(Parker Lab, Caltech)

Parker, speaking from his office, which is decorated in white decals of rove beetles — which his lab exclusively focuses on — said it pays to explore “obscure branches of the tree of life.”

Sceptobius has been living in the forest for millions of years, and humans have been inhabiting this part of the world for thousands of years, and it just took a 20-minute car ride into the forest to find this incredible evolutionary story that tells you so much about life on Earth,” he said. “And there must be many, many more stories just in the forest up the road.”

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John McCutcheon, a biology professor at Arizona State University, studies the symbiotic relationships between insects and the invisible bacteria that live inside their cells. So to him, the main characters in the recent paper are quite large.

McCutcheon, who was not involved with the study, called it “cool and interesting.”

“It suggests a model, which I think is certainly happening in other systems,” he said. “But I think the power of it is that it involves players, or organisms, you can see,” which makes it less abstract and easier to grasp.

Now, he said, people who study even smaller things can test the proposed model.

Noah Whiteman, a professor of molecular and cell biology at UC Berkeley, hailed the paper for demystifying a symbiotic relationship that has captivated scientists. People knew Sceptobius was able to masquerade as an ant, but they didn’t know how it pulled it off.

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“They take this system that’s been kind of a natural history curiosity for a long time, and they push it forward to try to understand how it evolved using the most up-to-date molecular tools,” he said, calling the project “beautiful and elegant.”

As for the broader claim — that highly dependent relationships become dead ends, evolutionarily speaking, “I would say that it’s still an open question.”

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