One of the clearest success stories in US healthcare over the past 20 years has been the dramatic decline in the number of Americans without health insurance. In 2010, the year the Affordable Care Act was enacted, 16 percent of the population lacked coverage. By 2025, according to estimates from the US government, that figure was cut nearly in half, to 8.3 percent.

The increase in coverage hasn’t been a panacea; even people with an insurance card can struggle to afford their medical bills or to secure a doctor’s appointment. But with the US standing alone among its international peers in its failure to offer universal healthcare, it represented significant progress toward ensuring every American had a basic level of access to routine medical services.

Now, however, those gains are about to be reversed.

Last year, when drafting their One Big Beautiful Bill, Republicans had a chance to strike a blow against the ACA — a law they’d vilified for years — 15 years after its passage and eight years after failing to repeal the law in President Donald Trump’s first term. They established work requirements to target the people covered by the ACA’s Medicaid expansion and allowed subsidies that had helped millions of people to buy private coverage on the ACA marketplaces to lapse.

As a result, millions of Americans are dropping their health insurance this year, and millions more are expected to lose their coverage in the years to come.

The uninsured rate has spiked before, but it’s usually the byproduct of an economic crisis; people lose their jobs, and they lose their coverage. What makes the current turmoil different is that it is entirely a matter of policy choices. 

Now, millions of Americans will pay the price.

“I don’t think there’s any historical precedent for the rollback in federal support for health coverage coming with the cuts in Medicaid plus the expiration of enhanced ACA premium subsidies,” Larry Levitt, executive vice president for health policy at the healthcare think tank KFF, told me. “The expected effects of OBBBA on coverage are self-inflicted and dwarf even the historical losses due to changes in the economy.”

ACA marketplace enrollment is projected to shrink dramatically in 2026

One of the major ways that the ACA expanded health insurance coverage was by setting up insurance marketplaces where individuals and families could purchase private health plans with the help of government subsidies.

Enrollment in those marketplaces has ballooned — particularly since 2021, when Democrats in Congress approved an expansion of the ACA’s financial aid that made more people eligible for assistance. Prior to 2021, there had been a strict cutoff at 400 percent of the federal poverty level (about $64,000 for an individual in 2026, or $132,000 for a family of four). Anybody who made a higher income was ineligible for aid. After 2021, anybody could qualify for ACA subsidies, and their insurance premiums were capped at a percentage of their income. (The subsidies were initially authorized for two years and, then, were extended to 2026 through the Inflation Reduction Act.)

It seemed to have plugged one of the obvious holes in the healthcare law: While many people below 400 percent of the poverty level had enjoyed both mandated comprehensive coverage and new government subsidies that offset any increases in costs, people above that threshold had been subjected to significant premium hikes since the ACA passed. Now, they were able to access the same subsidies, and sign-ups boomed. Marketplace enrollment grew from 9.8 million Americans in 2019 to 22.3 million in 2025. 

But, to keep down the cost of their legislation and get it passed with a narrow Senate majority, Democrats allowed the new subsidies to expire in 2026. Then, Trump won the 2024 presidential election, and Republicans took control of Congress. The GOP decided not to extend the subsidies, despite some bipartisan efforts to pull together a plan. When people went to sign up for their health insurance for 2026, many of them no longer had access to financial aid. I spoke last year with some of those people. One family was preparing to allow one parent and child to become uninsured so they could afford a health plan for the other parent who has an autoimmune disease. A young man with asthma also expected to go without coverage after his previous plan ($100 per month and no deductible) was no longer available, and the cheapest replacement he could find was $282 per month with a $10,000 deductible. He told me he was banking on being able to pay for his medication out of pocket or getting it through a charity service.

So, we knew some people would drop their insurance as a result of the expired subsidies, but it was hard to be sure how many. Now, we’re starting to get hard data, and it does not look good. Based on KFF’s preliminary analysis of enrollment data and premium payments, about 4.7 million fewer people will actually end up being enrolled in an ACA marketplace plan in 2026 compared to 2025 — a 21 percent drop in a single year.

Work requirements are going to knock millions of people off Medicaid

The ACA’s other major coverage provision was the expansion of Medicaid eligibility to any American with an income at or below 133 percent of the poverty level (about $21,000 for an individual in 2026, or $44,000 for a family of four). It replaced the preexisting patchwork system for eligibility that created significant differences across states — in particular, millions of childless adults, some of whom were living in deep poverty but had been left out of the program in many states before the ACA, now qualified for Medicaid. 

As of June 2025, more than 16 million Americans who became newly eligible for Medicaid through the ACA had been enrolled in the program, making up nearly a quarter of all Medicaid enrollees.

Republicans in Congress had been sharply critical of Medicaid expansion, even as many GOP-led states adopted it, and 2025’s OBBBA gave them a chance to roll it back. They approved, for the first time, national work requirements for Medicaid, targeted to expansion-eligible enrollees, and made several other technical changes to constrain states’ Medicaid financing. People on the program will be required to work or perform other approved activities for at least 80 hours per month or show they should be exempted from the requirement. Otherwise, they could lose their benefits.

And based on what we know from historical precedent, many of the coverage losses won’t be because people are actually ineligible for Medicaid, but because of the administrative burden of complying with these new requirements, even if you are working, or if you are someone — like a pregnant person — who is supposed to be exempted. Arkansas is the only state to implement Medicaid work requirements prior to the OBBBA, and only a fraction of the people required to submit work activities to the state actually did so; many of the people who lost coverage lost it because they failed to turn in paperwork. 

The Medicaid population is, by nature, hard to reach. This group is lower-income and might work irregular hours, move around more, or have less access to the internet. It’s easy for people to fall through the cracks.

The OBBBA’s requirements go into effect nationally in January 2027 (after this year’s midterm elections), but some states are instituting them early. Nebraska implemented work requirements on May 1, Montana and Arkansas are starting theirs on July 1, and Iowa will adopt the requirements on December 1. Then, starting on January 1, 2027, they will apply in every state.

The coverage losses are difficult to project, and they could take time to accrue, but they are expected to be sizable. The nonprofit research group RAND estimated Medicaid enrollment will drop by 7.6 million people by 2034. 

And they, much like those people dropping ACA coverage, will lose more than just their insurance card. Health insurance, even with its shortcomings, does a lot to help people. Americans with health insurance accrue less medical debt. They are more likely to go to routine medical appointments and receive routine screenings. Prior research on Medicaid expansion’s effects has estimated that it saved tens of thousands of lives.

In other words, the coming increase in the uninsured rate will do more than change some percentage points on a spreadsheet; it will make it harder for millions of Americans to stay healthy and stay alive.

Your immune system has one job: to protect you. And most of the time, it does that job like a pro. 

But occasionally it gets a bit overzealous, even paranoid. It mistakes harmless, even wonderful things—flowers, peanuts, cats—for threats, and attacks them (and you—mostly you) with a senseless, chaotic vengeance.

For most allergy sufferers, this might mean giving up a few tasty foods, staying inside during high pollen counts, or rehoming the cat—or, more realistically, the person allergic to the cat. But for a tiny number of people, the immune system decides to take aim at one of the most essential substances on earth: water.

Yes, it is possible to be allergic to water. And the condition is even stranger than it sounds.

“Imagine not being able to go into the pool, or the lake, or the ocean,” says dermatologist Dr. Amir Bajoghli, who has treated a patient with this rare condition. “My patient also has to take much faster showers, as you might imagine. It definitely interferes with quality of life.”

Yes, you can be allergic to water

The medical term for an allergy to water is aquagenic urticaria, a form of hives. The condition is so rare that only an estimated 100 to 150 cases have ever been reported. However, researchers believe many more cases go undiagnosed: When a patient comes in complaining of hives, “it could be water” is probably not the first thing that leaps to mind.

“Honestly, a lot of general physicians aren’t even aware of it,” says Bajohgli, an adjunct professor at Georgetown University School of Medicine. “It’s rare, and it’s not on their radar.”

Although scientists don’t fully understand exactly how aquagenic urticaria works, they believe water itself isn’t the culprit. Rather, it appears that certain people’s skin responds differently to water contact, setting off a reaction in the skin’s outermost layer. This triggers the body’s mast cells (immune cells that sound the alarm during allergic reactions), which releases histamine, the troublemaking chemical responsible for allergic responses. 

Within minutes of water touching the skin, a person with aquagenic urticaria will develop raised, intensely itchy welts. The reaction typically lasts anywhere from 30 minutes to an hour, and the longer the exposure, the more severe the symptoms.

You can still drink water, but sweating can be a problem

Interestingly, and luckily, aquagenic urticaria does not interfere with the body’s need for life-sustaining hydration. In other words, drinking water is fine. When water is swallowed and processed by the gut rather than absorbed through the skin, it doesn’t trigger the same immune response, Bajoghli says.

“The gut, just like the skin and the lungs, is one of the first forms of defense,” he says, “but in this case, somehow, it’s not eliciting the response in the gut the way it does in the skin.”

Bajoghli notes that some patients with aquagenic urticaria do react to their own sweat, although his patient does not. Sweat, he explains, involves an entirely different biological process than external water making contact with the skin.

Scientists believe an unidentified substance in the skin may be triggering this reaction, although much remains unknown. 

“It’s still, medically, for us, a mystery,” he says.

How to test if you’re allergic to water

For better or worse (mostly better), water is inescapable. Because of its ubiquity, and also because aquagenic urticaria is something of a medical unicorn, it often takes a while for patients or doctors to connect the dots. 

Once it occurs to the patient and provider that water could be the culprit, diagnostic testing is fairly straightforward. It typically involves applying water-soaked compresses to the skin and waiting. In most positive cases, symptoms appear within five minutes, although the test can take up to 30.

“We wait 30 minutes before we call it negative,” Bajoghli says.

The importance of very quick showers

So, what is life like for a person whose body treats H₂O as a sworn enemy? For Bajoghli’s patient, an active teenager involved in sports, the condition reshapes even the most basic daily routines. Among other things, this means really fast showers. 

“When he showers for about two minutes, the symptoms are more subdued and milder in nature,” Bajoghli says. “If he takes a longer shower, they’re more severe and they persist longer.”

The good news is that aquagenic urticaria is unlikely to cause a major allergic reaction. It is, however, chronic; patients should not expect it to resolve on its own.

Treatment options do exist, however. Bajoghli’s patient takes an antihistamine called cyproheptadine, which reduces symptoms enough to make that two-minute shower manageable. Timing is important: taking the antihistamine about an hour before water exposure helps maximize its effectiveness.

For patients who need more relief, Bajoghli says a newer drug called omalizumab has shown promise.

For now, the mechanisms behind aquagenic urticaria, including the identity of the substance—or antigen—that triggers it, remain poorly understood, and that knowledge gap makes it difficult to develop more targeted treatments.

“We’re really looking forward to finding out what that antigen is,” Bajoghli says, “and hopefully one day solving this.”

In Ask Us Anything, Popular Science answers your most outlandish, mind-burning questions, from the everyday things you’ve always wondered to the bizarre things you never thought to ask. Have something you’ve always wanted to know? Ask us.

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For a woman in her mid-40s to mid-50s, it arrives without warning. She wakes up, overheated, wondering why it’s so hot in the house—until she sees the thermostat is set for 70 degrees, same as always. Or, she’s midway through a work presentation when heat rises from her chest to her face, and she wonders if the flush on her cheeks is visible to everyone in the room. 

It’s a hot flash—a rite of passage for the majority of women in either perimenopause, the years leading up to menopause, or the years beyond it. Menopause itself is diagnosed after 12 consecutive months without a period, but the hot flashes don’t always get the memo.

Here’s everything doctors currently know about hot flashes.

What is a hot flash, and who gets them?

Hot flashes are a sudden heat flare up often paired with flushed skin and sweating. They don’t usually last long, between a minute and five minutes in duration.

Most women experience a hot flash about four and a half to five years after their last period, Dr. Monica Christmas, an OB/GYN at University of Chicago Medicine and director of its menopause program tells Popular Science. She also is the associate medical director of the nonprofit Menopause Society, which provides healthcare professionals with tools and resources to support women through the transition.

Women have grappled with hot flashes—whether simply annoying or genuinely debilitating—for centuries. In 1582, Dr. Jean Liebault of France was among the first to document the phenomenon. But while we know much more about hot flashes and night sweats than Liebault ever did, one question still stumps experts. 

“What we can’t answer is why doesn’t everybody get them,” Christmas says. “Because everybody doesn’t get them. I have patients that will say, ‘I don’t know,’ if I say, ‘Are you having any hot flashes or night sweats?’ And as soon as they say that, I’m like, ‘You’re not having them.’” 

What’s actually happening inside women’s bodies during a hot flash? 

During a hot flash, a woman might feel like she’s spiking a high fever, but physiologically, that’s not what is happening. As women approach menopause and the ovaries begin to make less estrogen, the brain’s internal thermostat—the hypothalamus—becomes hypersensitive to even small shifts in temperature, Christmas says.

The body “thinks” it’s overheating, even when the actual temperature hasn’t changed much. In response, our bodies try to cool us down. Blood vessels dilate, which is supposed to help dissipate some of that heat, but then that triggers a sweating reflex.

“Many people will say, ‘I feel this out of nowhere, this surge of warmth that typically is from the nipple line up,’” she says. “And then as soon as the heat came on, and I felt like I was internally heated up or on fire, I start to sweat.” 

How do women experience hot flashes differently? 

Exactly how an individual woman experiences hot flashes varies wildly. Some describe very mild symptoms. Others grapple with profuse sweating. Some experience only hot flashes during the day, while some have regular night sweats. About four in five women experience them at some point during the menopause transition, according to the American College of Obstetricians & Gynecologists.

“There’s a lot of variability,” Christmas says. Common triggers include alcohol, caffeine, high-sugar and highly processed foods, along with stress.

Black women also are more likely to experience more severe and longer-lasting symptoms, sometimes up to 11 years, she says. And research also shows that women with more severe, longer-lasting hot flashes and night sweats appear to be at higher risk of cardiovascular disease.

That doesn’t mean treating hot flashes automatically lowers heart risk, Christmas says. But it does reinforce that these women deserve particularly careful attention to blood pressure, cholesterol, and lifestyle. “I want to make sure I’m doing everything possible to minimize that risk,” she says when she treats her patients. 

There’s more to hot flashes than hormonal changes

For decades, the entire process was blamed purely on estrogen loss, Christmas says. But that explanation left some unanswered questions. 

“That doesn’t explain why every menopausal woman doesn’t have night sweats,” she says. “And it also doesn’t quite explain why we can sometimes start to experience them during the perimenopause transition because during perimenopause, people still have some estrogen.” 

Newer research now is telling a more complex story. When the brain recognizes that a woman’s estrogen levels are low, nerve cells in the hypothalamus called KNDy neurons (pronounced “candy”) become overactive, releasing neurotransmitters, which are chemical signals the brain uses to send messages throughout the body. These neurotransmitters include kisspeptin, dynorphin, and neurokinin B. 

“It’s actually those neurotransmitters that seem to have more of an impact on our ability to regulate our internal temperature,” Christmas says. “They’re not hormones.” 

What to do if you get a hot flash

For women in the middle of their hot flash years—along with the 10 percent of menopausal women who continue to experience them—there are treatments. 

Estrogen-based hormone therapy can help, but not every woman, including those with a history of blood clots or breast cancer, can take hormone therapy. 

Fortunately, researchers’ new understanding about the role of KNDy neurons has allowed for new treatments that block the brain signals that trigger hot flashes in the first place. The FDA approved a new drug called Veozah (it’s chemical name is fezolinetant) in 2023. It targets the neurokinin 3 receptor, which plays a key role in regulating body temperature. 

Lynkuet, another drug (with the chemical name elinzanetant), came along in 2025. It blocks both the neurokinin 1 and neurokinin 3 receptors, interrupting the process that triggers hot flashes at two points instead of one. 

Other medications can also provide relief, though weren’t originally developed for hot flashes, Christmas says. Some SSRIs and SNRIs; gabapentin, a neurologic medication; and oxybutynin, used for overactive bladder, are all used off-label for hot flashes and night sweats. 

Cognitive behavioral therapy and hypnosis also have been shown to reduce hot flashes. “I’m menopausal, too, so I know if I’m under a lot of stress or in a stressful situation, I’m going to probably have more hot flashes than not,” Christmas says. 

“So there’s certainly something about being able to calm our central nervous system down that seems to have an impact, too.”

If you’re struggling with hot flashes, Christmas recommends seeing your healthcare provider for help. Treatments are available. What’s more, in some cases, hot flashes or night sweats could signal other issues, including thyroid disorders, cancer, and infections, among others. 

But bottom line, when it comes to hot flashes, you don’t have to sweat them out.

In Ask Us Anything, Popular Science answers your most outlandish, mind-burning questions, from the everyday things you’ve always wondered to the bizarre things you never thought to ask. Have something you’ve always wanted to know? Ask us.

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Despite significant medical advances, spinal cord damage remains one of the most difficult physical injuries to treat. Scarring frequently gets in the way of nerve fiber regrowth, while nerve cells usually cannot regenerate on their own. A possible solution? A fleet of stem cell-infused, injectable nanorobots that can help nerve cells regenerate. The tiny bots are detailed in a study recently published in the journal Nature Materials.

To build their new tools, a team at ETH Zurich in Switzerland engineered microscopic machines that combine living neural progenitor cells (NPCs)—specialized stem cells developed for the spine—with customized nanoparticles. These customized nanoparticles feature two layers—one that is sensitive to magnetic fields and another that translates them into electrical signals.

“We place a reservoir in the center where we trap the cells. Then we inject the nanoparticles and wait for the two components to bind,” Salvador Pané i Vidal, a study co-author and ETH Zurich roboticist, said in a statement.

Each nanorobot is about six micrometers wide, making them smaller than a red blood cell. However, the number of robots required to pull off a procedure is immense. Millions of nanobots are needed during animal trials. Even with such a high number, the initial experimental results are promising. In tests involving mice with severed spinal cords, nerve cells stimulated by the microrobots began reconnecting at the injury site within 28 days. By the end of the trial, the mice displayed major improvements in movement, gait, coordination, and exploratory behavior. 

Significantly more research is required before these nanobots are ready for primetime, but the team hopes to one day begin testing similar devices in humans. Before that, they need to determine the most effective magnetic fields and how long to apply them to patients. In the meantime, the overall design could also be applied to help treat regenerative issues in organs and wounds.

“The reproducible and scalable production of microrobots using our lab-on-a-chip system demonstrates that the platform’s application potential extends beyond basic research,” added Pané i Vidal.

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In a family of killer diseases, pancreatic cancer has long been one of the scariest. It could grow undetected for years, and by the time most people knew something was wrong, their prognosis was grim. The vast majority of patients, nearly 90 percent, would die within the first five years of their diagnosis. Even as other cancers saw their mortality rates drop in recent years, pancreatic cancer’s death rate actually increased slightly from 1999 to 2020.

And despite their best efforts, scientists felt stuck. In the 1980s, they identified a gene, KRAS, that seemed to be pivotal to the uncontrolled cell growth that drove the disease’s development. But over and over again, most treatments in clinical trials failed. Dr. Anirban Maitra, director of NYU Langone’s Laura and Isaac Perlmutter Cancer Center and a longtime pancreatic cancer researcher, told me that pharmaceutical companies came to regard pancreatic cancer as a “graveyard” for future drug development. Experts feared the gene was, in effect, “undruggable,” Maitra said.

But recent breakthroughs have brought what once seemed impossible within reach. A group of researchers is preparing to publish results from their clinical trial, already reported in the New York Times, that found a KRAS-targeting pill called daraxonrasib roughly doubled survival, from seven months to 13 on average, among a group of patients who had metastatic pancreatic cancer and had already tried chemotherapy.

“For the first time, there is some optimism in this disease,” Maitra told me. “Oncologists who have been treating this cancer for decades have always been so pessimistic about the fact that so many trials have failed. These patients, unfortunately, live for a few months and die. But now we finally have the foundation on which to build.”

Effectively treating pancreatic cancer — or even possibly, some day, curing it — will ultimately demand more than one successful clinical trial. It’ll require improving the full spectrum of care, which means identifying who is at risk, detecting the disease early, and producing even more effective treatments that can offer patients hope of many more years to live, not just more months.

We are getting closer to being able to diagnose and treat pancreatic cancer with remarkable precision. Here’s what it will take to get all the way there — and what everyone should know.

Doctors are getting better at figuring out who’s at risk

One major problem with pancreatic cancer is that your pancreas is buried deep in your abdomen. You could have cancer growing there for years with no symptoms. Improving the outlook starts with detecting it early — and that work begins with figuring out who is most at risk.

Many people, and even doctors, may not be aware of what to look out for, Maitra told me. There have been some high-profile deaths that temporarily put the disease in the public eye — actor Patrick Swayze, tech titan Steve Jobs — but it hasn’t been the focus of major awareness campaigns like breast or even more recently colon cancer. Pancreatic cancer accounts for about 3 percent of all cancer cases — but more than 8 percent of cancer deaths, about 39,000 every year.

Smoking, age, and obesity are all considered to be risk factors — but that is something pancreatic cancer shares with many other types of cancer. One unique risk factor is the sudden onset of adult diabetes, especially when accompanied by weight loss, Maitra said.

“If you’re like a 65-year-old and you’re presenting with new-onset diabetes and you just lost 10 pounds, I would be very worried about that person. I’d make sure I get some tests done on that person,” Maitra said. “Awareness is so important.” He clarified that most new-onset diabetes in an adult is just that, and isn’t a reason to panic. Still, he said, the connection is something more people and health care providers should be aware of. 

New artificial intelligence programs could also help doctors identify who is most at risk. Hospitals are starting to experiment with scanning electronic health records or genetic samples, Maitra said, and singling out patients who may be at higher risk based on their medical history or the presence of certain genes that are associated with a greater chance of developing pancreatic cancer (including the breast cancer-causing gene BRCA2).

Clinicians have better tools for detecting pancreatic cancer early

Once doctors identify people who are at risk, they can deploy a host of new surveillance tools to look for pancreatic cancer’s development.

Blood tests, commonly referred to as liquid biopsies, have received a lot of investment, as well as media attention. Some companies aspire to create a test that could search for multiple cancers from one sample, but in the meantime, single-disease versions have shown promising if not quite ironclad results — including for pancreatic cancer. One blood test developed by Oregon Health & Science University had an 85 percent accuracy rate in diagnosing early-stage pancreatic cancer when it was used in tandem with an existing antigen test.

Once again, AI programs could help doctors get ahead of the disease. A recent study found that an AI program developed by Mayo Clinic researchers and used to examine routine abdominal CT imaging scans could spot pancreatic cancer at nearly double the detection rate of two human radiologists, finding the disease up to three years before a normal clinical diagnosis would occur.

“This is where AI can really help because they can pick out subtle patterns that the human eye can miss,” Maitra said.

Scientists are developing better pancreatic cancer treatments

Once doctors find the pancreatic cancer, they can treat it — and their options are getting better there too. 

Maitra said the best treatment remains surgical removal plus therapy — and the smaller the tumor, the better, which is why early detection is so essential. It also prevents the cancer from having more time to metastasize and spread.

Even after surgery, the cancer can come back. But new vaccines are showing promise in preventing that kind of recurrence; small preliminary studies have identified multiple vaccine candidates that allowed patients to live longer without a relapse and survive overall longer than the historical norms for pancreatic cancer patients.

And for the people facing the most dire scenario, when their cancer cannot be removed by surgery, that’s where the new treatments targeting KRAS — the gene that drives pancreatic cancer’s growth — could be a game-changer. 

To dramatically simplify the scientific breakthrough here, KRAS has been described by researchers as a “greasy ball” that for a long time no drug molecules were able to attach themselves to. As the Times reported, Kevan Shokat, a scientist at the University of California San Francisco, figured out how to make a molecule attach to KRAS in 2013; around the same time, Greg Verdine at Harvard University was working on a molecular “glue” that could disable KRAS. The new drugs build on this research to deliver a compound to the gene that can slow the out-of-control cell growth that causes pancreatic cancer.

But we should think of daraxonrasib, which seems likely to receive FDA approval, as the “ground floor” for this class of drugs, Maitra told me. Many people still do not respond to the treatment or experience severe side effects. The drug also stops working after a period of time, as people’s bodies develop a resistance to it. But other drugs that combine different molecules in an attempt to extend the treatment’s effectiveness are already in the pipeline. 

In the future, pancreatic cancer treatment could end up becoming a combination of all of the above: early detection, surgical removal to get the bulk of a tumor out, with vaccines and/or KRAS-based treatments used to prevent the cancer from coming back. And people who can’t undergo surgery for some reason might try a combination of vaccines and KRAS-targeting drugs.

The work is far from finished. But for the first time, after decades of disappointments, there is real reason for hope.