Scientists Find Possible Cause of Asthma, And How to Prevent an Attack

Imagine treating asthma not by suppressing symptoms—but by blocking the biological trigger that sets the entire storm in motion.

That’s no longer science fiction. In a discovery turning heads in respiratory medicine, researchers in the UK have found that a class of drugs once discarded in osteoporosis trials—calcilytics—may do something astonishing when applied directly to the lungs: they reverse the very mechanism behind asthma’s most crippling symptoms.

Let’s break this down.

In a groundbreaking study using both human airway tissue and mouse models, scientists at Cardiff University discovered that a protein called the calcium-sensing receptor (CaSR) plays a pivotal role in asthma.

When this receptor is activated—by environmental triggers like pollution, cigarette smoke, or pollen—it causes the airways to constrict, inflame, and become hypersensitive.

Enter calcilytics.

Originally developed to stimulate bone growth in osteoporosis patients, these drugs were shelved when they failed to deliver the hoped-for benefits.

But they were proven safe—and now, it seems, we just didn’t know where to aim them.

When calcilytics are nebulized directly into the lungs, they switch off the CaSR receptor.

The results?

According to lead researcher Dr. Daniela Riccardi, the asthma-like symptoms disappear—including airway twitchiness, inflammation, and the terrifying tightness that steals your breath.

“For the first time, we have found a link between airways inflammation—caused by allergens, smoke, or car fumes—and airway twitchiness in allergic asthma,” Riccardi says. “Our findings are incredibly exciting.”

And this is just the beginning.

Why Millions Still Suffer

Here’s the bitter truth: even though asthma is one of the most common chronic conditions on the planet, our toolbox for treating it hasn’t grown much in 50 years.

Roughly 1 in 12 people affected by asthma still can’t find a treatment that works.

That’s millions of people gasping through life, often depending on inhalers that offer only partial or temporary relief.

They’re not just managing symptoms—they’re battling uncertainty, every single day.

And yet, most current therapies target downstream effects—the inflammation, the spasms—not the trigger mechanism itself.

That’s what makes this research different.

This time, we’re looking upstream, at the root cause.

CaSR is like a panic switch in the lungs.

Flip it on, and everything spirals out of control.

Flip it off, and… calm.

This immediate, targeted approach could rewrite the rules of respiratory medicine—not just for asthma, but also for related conditions like COPD and chronic bronchitis, where inflammation and airway sensitivity are similarly destructive.

“This discovery enables us, for the first time, to tackle the underlying causes of asthma symptoms,” says Samantha Walker, Director of Research at Asthma UK. “If this proves successful, we may be just a few years away from a new treatment for asthma.”

What If the Problem Wasn’t Inflammation?

We’ve long accepted a narrative: that asthma is an inflammatory disease, full stop.

But what if that’s not quite right?

What if inflammation is the effect—not the cause?

This is the pattern interrupt.

Because Riccardi’s research suggests that CaSR activation comes first—triggered by environmental stimuli—and inflammation follows as a consequence.

In other words, we may have been treating the smoke instead of the fire.

This flips decades of asthma research on its head.

If CaSR is truly the switch, then controlling it means preventing the entire cascade: no twitchiness, no inflammation, no breathlessness.

The whole brutal cycle simply… doesn’t start.

And this reframing carries massive implications.

It shifts asthma from being a forever-managed condition to something potentially preventable.

That’s a seismic shift in thinking—and one that demands urgency.

“Asthma research is chronically underfunded,” Walker emphasizes. “We urgently need investment to take this to clinical trials.”

From Bone Failure to Breath Savior

So, how did a failed osteoporosis drug become a frontrunner in asthma research?

Calcilytics were developed about 15 years ago with the hope of strengthening bones.

By stimulating the release of parathyroid hormone through the calcium-sensing receptor, researchers hoped to reverse bone loss.

That didn’t pan out.

But here’s the twist: while calcilytics failed to deliver in bones, they turned out to be safe, well-tolerated, and minimally toxic—a rare combination in pharmacology.

So while their bone ambitions died, the molecule itself never went away.

And now it’s back—aimed at the lungs.

Administering calcilytics via inhalation bypasses the rest of the body, going straight to the site of the problem.

And in doing so, it blocks the asthma trigger at the source—before inflammation, before mucus production, before the wheeze.

“If we can prove that calcilytics are safe when administered directly to the lung in people,” Riccardi says, “then in five years we could be in a position to treat patients—and potentially stop asthma from happening in the first place.”

Let that sink in: stop it from happening.

The Road to Trials—and What Comes Next

Right now, Riccardi’s team is seeking funding for first-in-human trials.

The drug exists.

The pathway is known.

The challenge is proving that direct-to-lung administration is safe and effective in real-world patients.

That’s not a small ask.

Clinical trials take years, funding, and patient participation.

But unlike new molecules developed from scratch, calcilytics have already cleared major safety hurdles.

That could fast-track the process—potentially cutting a decade down to five years or less.

What does that mean for asthma patients?

It means we could see a paradigm shift in how we treat and even conceptualize respiratory illness.

Imagine not just managing symptoms—but turning off the disease switch.

This also opens doors for adjacent conditions. In COPD, bronchitis, and even chronic throat inflammation, the same CaSR pathway might be at play.

If so, calcilytics could become a multi-tool weapon in the fight against airway disease.