Nearly one in three people will experience an anxiety disorder at some point in their lives (Kessler et al. 2005). Rates of anxiety disorders, such as panic disorder, generalized anxiety disorder, and phobias, have surged over the last decade. A recent study documented a 300 percent rise in anxiety problems in American children between 2014 and 2023 (Gallagher et al. 2026).
The mainstream story is that anxiety is the product of a malfunctioning brain, rooted in an over‑excitable amygdala (LeDoux and Pine 2016). This alleged brain disorder, in turn, is shaped by faulty genes (e.g., Friligkou et al. 2024). Drugs like selective serotonin reuptake inhibitors (SSRIs) remain among the first‑line treatments.
But what if the problem isn’t anxiety, but the story we tell about anxiety? What if the “broken brain” story actually makes us more anxious by leading us to think that our anxiety is somehow hardwired into our genes and brains—and therefore can never be truly cured?
What if a new story, one that sees anxiety as a normal, healthy, and even purposeful part of human design, makes all the difference?
The Smoke Alarm Principle
A group of researchers from Cambridge just put that theory to the test. Led by Adam D. Hunt and Tom Carpenter, the team wanted to know how the stories we tell about anxiety actually affect patients’ lives. Do they help us get better, or do they make us worse?
To find out, Hunt and his team contrasted the mainstream genetic theory with a newer evolutionary theory. According to this evolutionary view, anxiety is an evolved defense—a kind of internal smoke alarm designed to protect us from danger (Nesse 2001).
Now, smoke alarms can differ in their sensitivity to combustion particles. (Anyone whose smoke alarm has gone off because of burnt toast knows this well.) When my smoke alarm goes off because I burn my toast, does that mean there’s a defect or dysfunction in the smoke alarm? Not at all. The smoke alarm is working exactly the way it’s designed to.
The same is true of our brains. Anxiety is an alarm signal—its job is to alert us to potential threats. In some people, because of a mix of genetic and environmental factors—such as adverse life experiences—the “anxiety knob” is set relatively high. Their brains are always scanning for potential danger.
But nothing inside of them is “broken.” From an evolutionary point of view, their brains are working just as designed.
In short, we can frame anxiety as a byproduct of a broken brain or as an evolved protective response. The question the new research asks is: Which one is better for sufferers?
Putting Genetic and Evolutionary Explanations to the Test
To answer this question, the research team gathered 171 practicing mental health clinicians across the United Kingdom and Ireland.
They split them into two groups. Group One was given a half‑hour video presentation that framed anxiety as a product of bad genes. Group Two was given the evolutionary theory, which framed anxiety as an evolved protective response.
The clinicians were then asked follow‑up questions: How optimistic were they that their patients could get better? What treatments would they recommend? How willing did they think patients would be to share a diagnosis?
The results were extraordinary. Clinicians who were given the evolutionary story were:
58 percent more likely to feel optimistic about patients’ recovery.
62 percent more likely to believe patients would be willing to share an anxiety diagnosis.
79 percent more likely to believe the public would seek psychiatric help if the evolutionary explanation were widely known.
62 percent more likely to believe psychosocial treatments, like cognitive-behavioral therapy (CBT) and exposure therapy, would be effective.
This is important because clinician optimism translates into patient success. Although they haven’t yet run this same experiment with patients, such an experiment is in the works.
Purpose, not Pathology
A paradigm shift needs to happen in how we understand and treat anxiety—one in which we see anxiety as a healthy, but perhaps exaggerated, evolutionary response. Yet too often, patients are told just the opposite: that their anxiety is a brain disorder to be managed with pills.
As lead author Hunt told me, “It’s frankly shocking how little exposure psychiatrists get to these sorts of normalizing explanations which make sense of uncomfortable emotions in terms of normal experiences which are going too far or not serving their purpose.”
There are many non‑drug therapies that remain the gold standard for anxiety, the main ones being CBT and exposure therapy. Hunt hopes that as people become aware of this evolutionary story, they’ll be more interested in exploring non‑medical alternatives: “One of the implications of taking an evolutionary perspective is that we should embrace environmental change as a first-line response.”
Hunt’s experiment adds to a growing body of research suggesting that the broken brain narrative—for example, the “chemical imbalance” theory of depression—may be doing more harm than good (see here and here). Seeing one’s problems as purposeful, rather than pathological, seems to lead to superior outcomes.
Yet this research raises a deeper question. If the brain disorder model is so harmful, why is it still the dominant story?
This is a question I tried to answer in my recent book. In the 1970s and ’80s, psychiatry underwent a biological revolution that saw mental health problems as brain disorders to be managed with pills. Though the evidence base for that biological narrative has crumbled, the narrative lives on—through a mix of professional inertia, vested pharmaceutical interests, and misguided anti-stigma campaigns.
Yet research like this gives us reason for hope. Unlike a normal smoke alarm, our evolved anxiety system can be recalibrated. Through techniques like CBT and exposure therapy, we can train our own brains to respond more accurately to threats.
This research suggests that the first step to changing our brains is to revise the story that we tell ourselves about anxiety. Anxiety may not be the result of a hypothetical brain or gene defect, but a highly designed system that can adapt and recalibrate.