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• Contrary to popular belief, there are many different kinds of dementia, each with its own unique symptom list.
• One of the most common forms of dementia that surfaces in midlife is called frontotemporal dementia (FTD); this is the form that Bruce Willis was diagnosed with.
• In a new study published in Nature Aging, researchers used spinal tap fluid to identify potential new biomarkers for FTD, which could lead personalized treatments.

While most people lump dementia into one general group, the truth is that there are different forms of the disease, each with their own symptoms.

The most common form of dementia that surfaces in midlife (generally talking 40s and 50s here) is called frontotemporal dementia (or FTD), and it tends to get confused with depression, schizophrenia, or Parkinson’s disease before people are properly diagnosed.

While Bruce Willis’ diagnosis with frontotemporal dementia has put a spotlight on this form of the devastating disease, there still aren’t any reliable biomarkers to detect or even monitor the condition.

But now, new research has helped to pinpoint certain changes that happen in the body due to frontotemporal dementia, and the findings could eventually lead to diagnostic testing for the condition. Here’s what the study found, plus what neurologists want you to know about early-onset dementia.

Meet the experts: Rowan Saloner, PhD, is a study co-author and professor in the UC San Francisco Memory and Aging Center; Clifford Segil, DO, is a neurologist at Providence Saint John’s Health Center in Santa Monica, CA; Amit Sachdev, MD, is the medical director in the Department of Neurology at Michigan State University

What did the study find?

The study, which was published in the journal Nature Aging, analyzed more than 4,000 proteins in spinal tap fluid from 116 patients with frontotemporal dementia. The researchers compared those proteins to ones from 39 of the patients’ healthy relatives.

The researchers discovered that patients with frontotemporal dementia had changes in the proteins that suggest they have problems with RNA regulation, which is required for the correct gene expression in the brain. (Gene expression can impact how your brain works.) These patients also had certain changes that impacted connections in their brains.

These proteins could be the first markers for frontotemporal dementia that surface when people develop the disease, according to the researchers.

Why are these proteins so important?

There are a few reasons. First, “frontotemporal dementia can be caused by several very different types of brain pathology, making it very difficult to provide an accurate diagnosis to patients,” explains Rowan Saloner, PhD, study co-author and professor in the UC San Francisco Memory and Aging Center. “Right now, we have no way to tell which pathology someone has while they’re alive, especially in non-inherited cases, which make up the majority of frontotemporal dementia.”

But by IDing changes in spinal fluid protein, doctors can detect the disease and track its progression. “That will hopefully lead to more accurate diagnoses and personalized treatments,” Saloner says.

That’s crucial, given that this form of dementia tends to be missed early on, says Clifford Segil, DO, a neurologist at Providence Saint John’s Health Center in Santa Monica, CA. But genetic testing could help give patients and their doctors a better sense of what might be behind their symptoms, he says.

One thing to keep in mind: This study focused on people with an inherited or genetic form of frontotemporal dementia. “We do not know if genetic frontotemporal dementia and sporadic frontotemporal dementia just look the same in the end but have different paths to development,” says Amit Sachdev, MD, MS, is the medical director in the Department of Neurology at Michigan State University. “If they have different paths, then this study has helped us learn about genetic frontotemporal dementia. That is useful but not as broadly applicable.”

What else do we know about early-onset dementia?

Early-onset dementias like frontotemporal dementia usually impact people in their 40s or 50s, Saloner says. “They can be difficult to diagnose, as early symptoms are often misattributed to stress or psychiatric disorders,” he says. “Compared to Alzheimer’s disease, which now has biomarkers and FDA-approved treatments, frontotemporal dementia remains behind.”

Segil says that early-onset dementia should be considered “if someone loses the ability to talk or express themselves and other neurological conditions like a stroke, seizure, or infection have been ruled out.”

Ultimately, Sachdev says that more information is better with the disease. “It is important to know as much as possible about how these diseases arise,” he says. “It gives us something to work from in everyone else.”

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Ah, it’s a lovely night for enjoying the outdoors. You go outside in the warm summer air to listen to the crickets and breathe in the scents of verdant life, and then turn your head to the heavens. You see hundreds of stars in the sky, and the brightest are conspicuously twinkling and gleaming.

Some are even shifting their colors across the rainbow, delighting your eyes and mind—unless you’re out there to do some observing with a telescope. That twinkling is lovely for any average stargazer to behold, but scientifically, it’s a pain in the astronomer.

Twinkling is the apparent rapid variation of brightness and color of the stars. It’s technically called scintillation, from the Latin for “sparkle,” which is apt. While it is admittedly lovely, it’s still the bane of astronomers across the world.

For millennia, twinkling was misunderstood. As with so many scientific principles, it was misdiagnosed by ancient Greeks such as Aristotle, who attributed it to human vision. At that time, he and his peers believed that the eye actively created vision by sending out beams that illuminated objects and allowed us to see them. But these beams were imperfect, so the belief went, and the farther away an object was, the more the beam would be distorted; stars, being very far away, suffered this flaw greatly, causing them to twinkle. It was Isaac Newton, through his studies of optics, who finally determined the true cause.

A fundamental property of light—true of all waves, in fact—is that it bends when it goes from one medium to another. You’re familiar with this: a spoon sitting in a glass of water looks bent at the top of the liquid. This is called refraction, and in the case of the spoon, it happens when the light goes from the water in the glass to the air on its way to your eye, distorting the shape of the otherwise unbent spoon. The amount of refraction depends on the properties of the materials through which the light travels. Density, for instance, can dictate the degree of refraction for light moving through gas—so light traveling through air alone will still bend if the air has different densities from one spot to the next.

If Earth’s atmosphere were perfectly static and homogeneous, then the refraction of starlight would be minimal. Our air is always in motion, however, and far from smooth. Winds far above the planet’s surface stir the air, creating turbulence. This roils the gases, creating small air packets of different densities that move to and fro.

Starlight passing through one such parcel of air will bend slightly. From our point of view on Earth, the position of the star will shift slightly when that happens. The air is also in motion, so from moment to moment, the starlight will pass through different parcels on its way to your eye or your detector, shifting position each time, usually randomly because of the air’s turbulent motion. What you see on the ground, then, is the star rapidly shifting left, right, up and down, and all directions in between, several times per second—in other words, twinkling.

The amount of the shift is confusingly called “seeing” by astronomers, and it’s actually quite small. It’s usually only a few arcseconds, a very small angle on the sky—the full moon, for example, is about 1,800 arcseconds wide. Stars, though, are so far away from us that they appear to be a minuscule fraction of an arcsecond wide, a tiny point of light to the eye, so even this minuscule arcsecond-scale shifting makes them appear to dance around.

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I am standing outside an ordinary house in a tree-lined street on a midsummer afternoon, about to change my life. I glance through a  window and see the reassuring domestic ephemera of books, a computer monitor, a child’s drawing. Next to the front door is a small, typed sign with the details of a psychotherapist. I draw myself up, feeling both grown up and childishly nervous, and ring the buzzer.

It is June 2012, and I am nearing 38. The country is preoccupied with whether the Olympics will be ready on time and if England might crash out of the Euros. I have other things on my mind. A few weeks earlier, I made a call. The woman on the end of the line was polite, warm, and to the point, and we agreed to meet. Waiting for her to answer the door, I start to sweat: will I like her? Will she think I am a time-waster? What am I going to say?

I feel like an outlier: in 2012, therapy carries something of a stigma. Beyond one or two close friends, I haven’t told anyone I’m here. The open conversations we have today around mental health weren’t happening. Now, Covid has sharpened everyone’s awareness of their own mental health struggles: according to a report by Mind last November, over a third of Britons say they don’t have the support or tools to deal with the ups and downs of life. Ten million people will need support for their mental health as

a direct result of the pandemic, according to the Centre for Mental Health. Demand for therapy is outstripping supply. A study by the New York Times in December 2021 revealed that therapists in the US, where it has always been more accepted, are turning away patients. Even in the UK, demand for mental health advice has soared since the start of the pandemic.

It hasn’t taken a crisis for me to seek help. I’m doing so because I feel stuck: at work, in life, and certainly in love. I feel there is a braver, happier, more fulfilled person inside me trying to get out, but I don’t know how to reach her. I am existing with a low-level frustration, without being able to pinpoint what I am frustrated with, let alone find the tools to address it.

I have been wondering for a while if talking to a professional might help. But something has always stopped me: who am I, with a loving family, good friends, a roof over my head, and food on the table, to need therapy? I don’t come from a family of therapy-seekers. My Yorkshire-born parents, from working-class homes, would no sooner have sought out something so self-indulgent than joined a circus. In the world I’ve grown up in, therapy is seen as a  rather shameful last resort for someone in need of help, not for someone with a functioning life who’s feeling a bit directionless. Just cheer up and get on with it was the message I learned.

As a result, it has taken me a long time to convince myself that, even though I am not suffering from what my friend (and also a therapist), Ellen, calls “capital T trauma”, it could be helpful. As Stephen Grosz writes in his 2013 book The Examined Life: “At one time or another, most of us have felt trapped by things we find ourselves thinking or doing, caught by our own impulses or foolish choices; ensnared in some unhappiness or fear; imprisoned by our own history. We feel unable to go forward, and yet we believe that there must be a way.”

I want to change. In fact, I want to be a different person altogether. I am like an old house whose electrics keep shorting in the same place, and I want someone to rewire me. I have a very strong sense that unless I do something, I’ll be stuck here for ever. So here I am, sweating on a doorstep, asking for help. I am about to learn a huge amount.

Tears Are Useful

As I sit down for my first session, I notice a box of tissues on a table within arm’s reach. I get through a lot of them that afternoon. The release of talking, of being listened to, is an emotional experience.

We sit in a book-filled room; I am on a comfy sofa, my therapist is on a chair. Light pours in. Over the years, I can almost memorise the titles behind her, so long will I spend gazing at them when stuck for words. Likewise, the tree outside her window becomes as familiar as the view from my own flat: I will witness its full cycle – from summer fullness to bare winter branches – many times over.

In these early weeks, I do a lot of talking as my therapist gets to know me. When she speaks, it is often to affirm what I’ve said: “It sounds like you’ve always … ” or, “It’s OK to feel … ” At first, I sit upright; as I start to feel more comfortable, I sometimes curl my legs under me.

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Images of inhumanity and atrocity are burned into our memories. Jewish men, women, and children being herded into gas chambers. Entire villages destroyed by rampaging gangs in Rwanda. The systematic use of rape and the destruction of communities as part of ethnic cleansing in the Balkans. The massacre at My Lai in South Vietnam, the abuse of Iraqi prisoners in Abu Ghraib, and most recently, the carnage wrought by suicide bombers in Baghdad, Jerusalem, London, and Madrid. Reflecting on these events, we inevitably ask: What makes people so brutal? Are they mentally ill? Are they the products of dysfunctional families or cultures? Or, more disturbingly, is anyone capable of taking part in collective ruthlessness given the right–or rather, the wrong–circumstances? Now, the latest research, including possibly the largest social-psychology experiment in three decades, is providing a new window on these conundrums.

Initially, theorists sought answers to group pathology in individual psychology. In 1961, however, German-born American historian and political philosopher Hannah Arendt witnessed the trial in Jerusalem of Adolf Eichmann, one of the chief architects of the Holocaust. She concluded that far from the defendant demonstrating a perverted and sadistic personality (as psychiatrists for the prosecution claimed), he was utterly unremarkable and disarmingly ordinary. Arendt pronounced Eichmann to be an embodiment of the banality of evil.

Everyday Evil?

First published in 1963 in the New Yorker, Arendt’s analysis was considered shocking and heretical. But a series of studies conducted around the same time supported her observations. In experiments at U.S. summer camps during the late 1950s, Muzafer Sherif, a Turkish-born American social psychologist, learned that normal schoolboys became cruel and aggressive toward former friends once they had been placed in different groups that had to compete over scarce resources. Even more striking were obedience studies carried out at Yale University in the early 1960s by Stanley Milgram. Ordinary, well-adjusted males who took part in a bogus memory experiment were told to deliver electric shocks of increasing magnitude to another person who posed as the learner. (In actuality, the learner, an accomplice of the experimenter, received no shocks.) Amazingly, every single teacher was prepared to administer intense shocks of 300 volts, and two thirds obeyed all the experimenter’s requests, dispensing what they believed were 450 volts. Participants continued meting out punishments even after hearing the learner complain of a heart condition and yell in apparent agony. Milgram concluded: Arendt’s conception of the banality of evil comes closer to the truth than one might dare to imagine.

The vivid culmination of this line of inquiry was the Stanford prison experiment, carried out in 1971 by Stanford University psychologist Philip G. Zimbardo and his colleagues. The researchers randomly assigned college students to be either prisoners or guards in a simulated prison in the basement of the campus psychology building. The goal was to explore the dynamics that developed within and between the groups over a two-week period. The study delivered these dynamics in abundance. Indeed, the guards (with Zimbardo as their superintendent) exerted force with such harshness that the study was halted after only six days.

The experimenters concluded that group members cannot resist the pressure of their assumed stations and that brutality is the natural expression of roles associated with groups who have unequal power. Accordingly, two maxims, which have had immense influence at both a scientific and a cultural level–and which are taught as received knowledge to millions of students around the world every year–are routinely drawn from the Stanford experiment. The first is that individuals lose their capacity for intellectual and moral judgment in groups; hence, groups are inherently dangerous. The second is that there is an inevitable impetus for people to act tyrannically once they are put in groups and given power.

Reexamining Group Power

The weight of the Stanford prison experiment lies in both its dramatic findings and the simple, stark conclusions that have been drawn from it. Over the years, however, social psychologists have developed doubts about the resulting received wisdom.

First, the idea that groups with power automatically become tyrannical ignores the active leadership that the experimenters provided. Zimbardo told his guards: You can create in the prisoners… a sense of fear to some degree, you can create a notion of arbitrariness that their life is totally controlled by us…. Theyll have no freedom of action, they can do nothing, say nothing that we dont permit…. Were going to take away their individuality in various ways.

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Have you ever done a deep clean of your fridge and noticed that the shelf doors have essentially turned into time capsules stashing condiments way past their expiration dates?

Obviously, it’s time to toss the mystery mayo that’s leftover from a long-ago barbecue and the forgotten-about jar of salsa that’s turned into a science experiment. But there are all kinds of other scenarios that are more befuddling: Do you need to get rid of the sour cream that has a pool of liquid on top of it, but hasn’t reached

its expiration date? (You’ve probably got a couple days, btw, but the end is nearing for your taco topping). And what about ketchup and mustard from last summer’s cookouts?

If you find yourself in a condiment conundrum, and you’re deciding what to toss and what to keep, there are a few general rules to be mindful of, says nutritionist Mary Sabat, MS, RDN, LD.

First things first: Is the bottle opened? Unopened condiments are generally going to have a longer shelf life compared to open ones since they haven’t been exposed to potential contaminants that can speed up bacteria growth, Sabat says.

“Once a bottle is opened, the shelf life can be significantly reduced due to increased exposure to bacteria,” Sabat says.

Proper storage is also a biggie. Many condiments need to be stored in a cool, dry place away from sunlight and heat, while refrigeration is necessary for things like mayo and creamy salad dressings that will otherwise spoil.

Expiration dates printed on the condiment bottles are really meant to tell you when the product is at its peak quality, Sabat says. Expired sauces, spreads, and dressings will likely lose their flavor over time, and, worst-case scenario, could make you sick.

With that info out of the way, here are 13 condiments you should never eat after their expiration dates (and in some cases, may even need to toss earlier).

Mayo Needs to Be Tossed Two Months After Opening

A safe rule of thumb is anything that contains mayonnaise should be tossed at the time of its expiration, especially if the jar has been opened, says dietitian Bess Berger, RDN, with the New Jersey-based company Nutrition by Bess.

Store-bought mayo usually contains acids which help prevent spoilage and kill off bacteria. But you may need to toss a half-full bottle of mayo before its expiration date if it’s been sitting out in the sun all day during a backyard barbecue, Berger says. Also, after it’s opened, it should go in the fridge for up to two months, according to the USDA.

Keep Close Tabs on Mayo-Based Dips, Too

From garlic aioli to remoulade and tartar sauces, there are all kinds of dipping sauces and spreads that contain mayo, and Berger says it’s best practice to toss them when they’re expired.

“Another general rule of thumb is if a dip or condiment tastes different from when you first open it, throw it out,” she says. “Same holds true if it’s discolored or extra watery.”

Horseradish Loses Its Zing

“As soon as the jar of horseradish is exposed to air, that sharp, spicy flavor begins to fade,” says Jared Kent, a sous chef at Good Roots in Akron, Ohio. By the time it reaches the expiration date, it’s better to opt for a fresh jar and get the whole experience, he says.

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Hannah Arendt has been on my mind a lot lately. The 20th-century German-Jewish political philosopher escaped the Nazi Holocaust, and won regard as one of the world’s greatest public intellectuals at a time when few women were appointed to university faculties. She drew on history, literature, and her own life to identify the conditions under which open and liberal societies turn into authoritarian states. Seven decades ago she made observations that still offer powerful insights today.

In The Origins of Totalitarianism, Arendtemphasized one primary factor in the rise of authoritarianism that has little obvious connection to politics: loneliness. While we usually think of loneliness as not having our social needs met, Arendt defined the word as something deeper. Loneliness happens when there are no shared objective facts and no potential collective action to solve shared challenges. It’s a state of being where you can’t trust others. Loneliness, in Arendt’s telling, inflames the connective tissues of a society. It weakens the body politic so that demagogues and despots can prey. “What prepares men for totalitarian domination,” she wrote, “… is the fact that loneliness, once a borderline experience usually suffered in certain marginal social conditions like old age, has become an everyday experience.”

Arendt—as far as I know—didn’t use the word “inflammation” to describe the effects of social isolation on a country or culture. But it’s the metaphor that, to me, gets to the essence of her warning.

Inflammation is the body’s response to a sense of threat—a protective, contractionary response that can extend even to the cellular level. It’s a response that can inhibit healing. A community or society that faces a deficit of meaningful connectedness is similarly in a state of perpetual threat; people are unable to listen to one another, to trust each other, to maintain trust in shared institutions, or to collectively overcome divisions.

This might sound familiar.

From 2003 to 2022, face-to-face socializing among U.S. men fell by 30 percent. For teenagers, it was a staggering 45 percent. An estimated 12 percent of Americans report having no close friends, a fourfold increase since 1990. While social media was supposed to amplify human connection, the rise of comparison culture, social sorting into echo chambers, and the rapid decline of in-person social connection have instead coincided with unprecedented levels of anxiety, depression, and distrust.

It should therefore come as no surprise that, in America, we’re seeing democratic backsliding like Hannah Arendt warned of—including mass polarization, intentional disinformation, and a politics of fear, retribution and rage.

Loneliness inflames societies.

It just so happens that loneliness inflames the body, too.

Two decades ago, researchers Louise Hawkley and John Cacioppo at the University of Chicago demonstrated in a landmark study that loneliness acts as a chronic stressor that triggers the body’s innate stress-response systems. Social isolation keeps the hypothalamic-pituitary-adrenal (HPA) axis in a constant state of arousal, driving persistent cortisol release. This hormonal imbalance heightens inflammation. And this can, in turn, weaken the immune system, compromise cardiovascular health, and worsen vulnerability to mental health conditions such as depression and anxiety. In short, the absence of meaningful social bonds can literally recalibrate the body’s physiological mechanisms toward greater stress and illness.

Over the past two decades, further studies have only reinforced the link between loneliness and inflammatory pathways. George Slavich of the University of California, Los Angeles, underscores that experiencing social disconnection can mimic physical threats in how our brains and immune

systems respond, magnifying the release of inflammatory agents. From an evolutionary standpoint, sustained isolation disrupts our primal need for social integration, leading to inflammation and a whole host of downstream consequences.

It’s easy to downplay the loneliness problem. When former U.S. surgeon general Vivek Murthy warned of the dangers of social isolation and proposed solutions, no meaningful government interventions ensued. Likewise, when the U.K. government appointed a minister for loneliness in 2018, many likened the move to a Monty Python sketch rather than seeing it as a serious policy intervention.

But the medical, social, and even political costs of growing social isolation mean that we can no longer afford to ignore it.

Some solutions are straightforward. Medical innovators are now addressing social isolation through practices like “social prescribing,”—wherein health professionals connect patients who are lonely with nonmedical community services, volunteer programs, exercise groups, and arts activities to improve their well-being. Instead of writing prescriptions for pills, doctors can prescribe a free pass to a museum, an invitation to join a gardening club, or a support group for people facing similar struggles. A recent multiyear evaluation of nature-oriented social prescribing in the U.K. found that programs significantly helped participants reduce anxiety and improve happiness.

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If you live anywhere affected by the recent heatwaves, you may well have spent your nights tossing and turning, trying out different sleeping positions in an attempt to get comfortable. But what does the evidence say about which sleeping positions are actually the best?

Studies on everyone from seafarers on container ships to welders in Nigeria might be able to help us, although given how important sleep is to us it’s surprising how few large-scale studies have been conducted.

First you need a way of working out which position people are sleeping in. You can ask them of course, but we only really remember the way we were lying when we were trying to fall asleep and the position we wake up in. To find out more, researchers have tried a variety of techniques including filming people while they sleep or getting them to use wearable technology that monitors their movements.

In Hong Kong, researchers are developing what they call the “Blanket Accommodative Sleep Posture Classification System”, which uses infrared depth cameras that can detect a person’s sleep position even through a thick blanket.

Researchers in Denmark used small motion-sensor detectors attached to volunteers’ thighs, upper backs, and upper arms before they went to sleep to establish their favoured sleeping position. They found that during their time in bed, people spent just over half their time on their sides, around 38% on their backs, and 7% on their fronts. The older the people were, the more time they spent on their sides. 

This bias towards sleeping on our sides is something we develop only as we become adults, because children over the age of three spend on average an equal amount of time sleeping on their sides, back and fronts.

Babies, meanwhile, sleep mainly on their backs because they’re put in their cots this way for safety reasons.

So sleeping on your side is the most common position, and we could trust the wisdom of the crowd to choose the position where they sleep best, but what about the data? A very small observational study in which people could sleep however they preferred found that those who slept on their right side slept slightly better than those on their left, followed by those on their backs.

If you find it easy to sleep on your side, then it’s probably also best for anyone else trying to get to sleep nearby. On one occasion, while touring a submarine for a radio programme I was making, the submariners showed me their sleeping quarters, where the bunks were stacked so closely on top of each other that it was hard to turn over. That meant they tended to sleep on their backs, so they told me it was a race to get to sleep first before the whole cabin was full of snoring men.

Another small study looked at seafarers working on merchant container ships and found that respiratory disturbances such as snoring were more common when the seafarers were sleeping on their backs.

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Scientific research over the past 30 years has revealed a patchwork of potential causes of autism. Most of them are genetic—the condition is between 60 and 90 percent heritable—and some involve nongenetic risk factors that might impact development during pregnancy.

“We’ve found a great deal of the underlying [causes],” says Helen Tager-Flusberg, an autism researcher and a professor emerita at Boston University. But how these different risk factors come together as the brain develops remains a challenge to piece together. “Autism is not a simple disorder,” she says. “There are no simple answers. There are no so-called smoking guns.”

Even so, Robert F. Kennedy, Jr., the U.S. secretary of health and human services, talks about autism in a way that suggests he thinks there are simple and direct causes. He often refers to the steady rise in autism prevalence (which is likely due to improved screening and diagnosis) as an indicator that

we’re in the middle of an “autism epidemic” driven by “environmental toxins.” He has also refused to disavow the long-debunked idea that vaccines cause autism. This month, as part of Kennedy’s effort to find “the root causes of autism,” the National Institutes of Health and the Centers for Medicare & Medicaid Services announced that they will create a “data platform” to study the condition. In April, NIH Director Jay Bhattacharya had described plans for “national disease registries, including a new one for autism.” The plan involved collecting “comprehensive” private health data on autism that would represent “broad coverage” of the U.S. population, leading autism advocacy organizations, civil rights groups, and research scientists to warn of medical privacy concerns. (Shortly after outlets reported on Bhattacharya’s statements in April, HHS denied that it planned to create an “autism registry.”)

In a budget hearing on Wednesday, Kennedy called for an end to genetic research into autism. “I don’t think we should be funding that genetic work anymore,” he said. “What we really need to do now is to identify the environmental toxins.”

In response to this dismissal of well-established science, Tager-Flusberg has organized a coalition of scientists to push back. The Coalition of Autism Scientists now has 258 members and is still growing.

Scientific American spoke with Tager-Flusberg about Kennedy’s statements this week and how the autism community is responding.

In a Congressional budget hearing Wednesday afternoon, Robert F. Kennedy, Jr., said: “Autism is an epidemic, and the genes do not cause epidemics. They can contribute a vulnerability, but you need an environmental toxin. It’s like cigarettes and smoking.” What was your reaction to that?

There is no reason that we need to refer to the increased prevalence rates, which have been rising steadily for many years now, as an epidemic. This is not the definition of an epidemic, so I take issue with highlighting that.

Second of all, genetics are the primary contributing factor to autism. We know specific genes and variants confer increased risk, even in cases where there aren’t any clear environmental contributions. If anything, it’s the other way around—it’s the environmental factors that add to or interact with the genetic risk for autism.

Take one of the very well-regulated nongenetic factors: parental age, particularly paternal age. What we think is going on is that, as parents age, their germ cells [which develop into eggs or sperm] are changing, and so this is leading to alterations in the DNA that then confer risk for autism.

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Ellen Stromdahl was at a garden party in coastal Virginia in June 2023 when her friend Albert Duncan stood up from where he was sitting and abruptly fainted. Duncan is an outdoorsman in his mid-80s — still active and healthy for his age. Stromdahl, an entomologist who works for the United States Army Public Health Center, the Army’s public health arm, rushed to his side. As Duncan came to, she noticed that his tanned skin was tinged with yellow. “This man looks jaundiced,” she thought to herself.

Duncan spent the next several days in and out of the emergency room. His doctors administered countless blood tests and ruled out the usual suspects for an octogenarian — heart disease, diabetes, pneumonia. Finally, on Stromdahl’s recommendation, Duncan’s wife, Nancy, asked his doctors to test him for babesiosis, a rare malaria-like disease caused by microscopic parasites carried by black-legged ticks. The test came back positive not just for babesiosis but also for Lyme disease, another far more common illness caused by the same type of tick.

If Duncan’s doctors had caught the infections sooner, they could have eradicated them with a combination of oral antibiotics and antiparasitic medications. But Duncan, weeks into his illness, needed a procedure called an exchange transfusion. Doctors pumped all of the infected blood out of his body and replaced it with donor blood. About two weeks after the garden party, he was well again.

Babesiosis is rare — the Centers for Disease Control and Prevention reports around 2,000 cases in the United States every year. But what made Duncan’s case even more unusual is that he contracted babesiosis in Virginia, a state that registered just 17 locally acquired cases of the disease between 2016 and 2023.

It got Stromdahl wondering if babesiosis could be becoming more common in Virginia and neighboring states. She spent the following two years working with a team of 21 tick researchers from across the eastern U.S. and South Africa to assess the prevalence of Babesia microti, the parasite that causes babesiosis, in ticks and humans in those states from 2009 to 2024.

The results of the study, published in April in the Journal of Medical Entomology, reveal that the Babesia parasite is rapidly expanding through the mid-Atlantic. This shift, which has coincided with changing weather patterns, could pose a serious threat to people in communities where the disease has long been considered rare.

“Wherever we found positive ticks, there were cases,” Stromdahl said. “They’re small numbers, but that’s why we want to give the early warning before more people get sick.”

One in four cases of babesiosis is asymptomatic. People who do develop symptoms, especially older adults and immunocompromised people, can get quite sick with fever, chills, anemia, fatigue, and jaundice. Untreated, the parasites, which infect and destroy red blood cells, can lead to organ failure and death.

Babesiosis is typically found in the Northeast and the Upper Midwest. Between 2015 and 2022, case counts in the states that regularly report the disease — Connecticut, Massachusetts, Minnesota, New Jersey, New York, Rhode Island, and Wisconsin — rose by 9 percent every year, a development researchers attribute in large part to warmer temperatures caused by climate change, which afford black-legged ticks more opportunities to bite people in a given year and more habitat to spread into.

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