Funks SwabbieMany people have lived through physical pain all their lives, but not this woman, Jo Cameron from Scotland. For Jo Cameron, pain has been mostly optional. She has walked through burns, surgery, broken bones and childbirth with a calm that baffled doctors and intrigued scientists. Her case has opened a rare window into how the body controls pain, mood, and healing—and it has sparked hopes for new treatments that could help millions.
This is the story of how a quiet Scottish woman came to occupy an outsized place in neuroscience, what researchers discovered about the genes that shaped her experience, and what her life reveals about the costs and benefits of living with muted pain.
A life of “odd” recoveries
Joanne “Jo” Cameron grew up and lived most of her life in rural Scotland. To neighbors and friends she was a teacher and an ordinary person. What set her apart, at least when doctors finally noticed, was how she handled injury.
She had lived through serious events without the usual aftermath. When she broke bones as a child, she recovered quickly and without the prolonged suffering many would expect. She endured burns and operations with little or no pain medication. In one striking episode, she received hand and hip surgery and reportedly required far less anaesthesia and analgesia than anyone thought necessary. Those who treated her began to suspect that something in her biology was different.
That “something” drew researchers. In 2013 a practicing doctor alerted geneticists to a patient who appeared unusually pain-resistant. The trail led to University College London and other research groups who took blood samples and sequenced parts of Jo’s genome. The results were surprising: she carried unusual variants near a gene linked to the endocannabinoid system — a biochemical network involved in pain, mood and memory. The discovery suggested that Jo’s painless life was not a myth or bravado. It had a molecular trace.
What scientists found: FAAH, FAAH-OUT and the endocannabinoid system
The first reports on Jo’s biology emphasized changes affecting FAAH — short for fatty acid amide hydrolase — an enzyme that breaks down endocannabinoids, the body’s own cannabis-like chemicals. One of those chemicals, anandamide, binds to cannabinoid receptors in the brain and body and reduces pain, eases anxiety and impacts memory and appetite. If FAAH works less efficiently, anandamide can linger longer, amplifying those calming effects.
Jo turned out to have a rare combination: a common point mutation that reduces FAAH activity and, crucially, a second anomaly in a nearby non-coding region dubbed FAAH-OUT — a pseudogene-like sequence that appears to control how FAAH is expressed. The result: higher levels of anandamide and related molecules, blunted pain signaling, faster wound healing and lower anxiety.
Early reports described the effects in human terms. Jo remembered childbirth as uncomfortable but not painful. She spoke of surgeries she “didn’t feel” in the usual way and of an odd sense that wounds healed quickly. Interviews noted that she sometimes seemed carefree in ways her friends found unusual. Those biographical details gave laboratory results a human face: this was not only a biochemical curiosity but an ordinary life altered at a deep, sensory level.
Why the finding matters
Pain medicine has been at an impasse for years. Opioids remain a powerful tool for acute and chronic pain, but they carry high risks of addiction and side effects. Non-opioid options often fail to provide adequate relief. Finding new molecular targets has been a priority, and nature occasionally provides clues: rare people who feel little pain have pointed science toward channels and pathways that could be exploited safely.
Jo’s case added a fresh candidate. The FAAH enzyme and the endocannabinoid system already attracted interest from pharmacologists. Drugs that block FAAH should — in principle — increase anandamide and reduce pain, anxiety and perhaps improve healing. In Jo’s biology, researchers saw a natural version of an approach they had long considered. Studying her gave scientists a chance to test hypotheses about long-term effects, safety and the broader behavioral consequences of shifting this chemical balance.
Importantly, Jo’s mutations were not simply a binary “no pain” switch. Her case appears subtler: she does not lack all pain sensation, and she does not show the dangerous self-injurious behaviors sometimes seen in congenital pain insensitivity syndromes. Instead, she seems buffered against extreme pain and against anxiety. That distinction matters for drug design. A therapy that mimics Jo’s profile — reducing pain while preserving protective sensation — could be a game changer.
Not the only path to painlessness
Cases like Jo’s are rare but not unique. Researchers have catalogued several genes tied to severe pain disorders — for example mutations in SCN9A (which affect the NaV1.7 sodium channel) can produce congenital insensitivity to pain, while changes in PRDM12 or ZFHX2 have been linked to other forms of altered perception. What differentiates Jo’s story is the particular involvement of the endocannabinoid system and the fact that her life did not show the dramatic negative consequences that sometimes accompany total loss of pain.
This is a reminder of how many biological routes exist to similar outward effects. Some pathways remove nociceptors (pain receptors) themselves; others alter signalling downstream. Jo’s pattern — a modulation of an endogenous chemical system that tempers pain and anxiety while preserving protective reflexes — may be especially promising because it suggests a tunable target rather than an all-or-nothing outcome.
The human side: how Jo remembers and lives with her difference
Media profiles of Jo emphasize a calm presence and a wry sense of humor. She described childhood incidents — scalding, fractures — that other people found painful but she recalls as survivable. Colleagues and local reporters painted a picture of a woman who never sought attention for her condition. She lived quietly, teaching and gardening, until clinicians studied her more formally.
Interviews also cover less obvious consequences. Mutations that reduce pain tend to influence other domains: mood, memory and social behavior. Jo’s high levels of endocannabinoids may partly explain reports of lower anxiety and a sunnier disposition. But scientists caution against oversimplifying. The endocannabinoid system touches many neural circuits, and its chronic up-tuning can produce complex effects. What looks like “fearlessness” to strangers can also alter how a person perceives risk and how they respond to stressors.
Still, Jo’s life provided no evidence of reckless self-harm or inability to navigate daily life. That distinguishes her case from more severe congenital insensitivity disorders and suggests that a measured change in this system might be therapeutically useful.
Cautionary notes from the lab
When the first wave of media coverage hit in 2019, drug companies and research labs were alert. A cautionary episode from earlier attempts to translate FAAH inhibitors into drugs remains instructive. In 2016, a clinical trial of a FAAH inhibitor in France triggered severe adverse reactions in healthy volunteers, including one death. That catastrophe chilled FAAH inhibitor development and showed the risks of interfering with complex neural chemistry.
Researchers studying Jo emphasize a careful approach. Her biology is intricate: it includes genetic variants in regulatory regions (FAAH-OUT) that modify enzyme expression in ways not easily replicated by a single drug. Moreover, the long-term effects of elevated endocannabinoids in the brain remain incompletely understood. Any therapeutic strategy inspired by Jo’s case must account for safety, dosage, and the possibility of unintended cognitive or emotional consequences.
New research and evolving understanding
Science did not stop at the first discovery. In the years that followed, teams continued to probe how FAAH-OUT and related genetic elements regulate FAAH and the broader endocannabinoid system. A more recent wave of research has used cell lines, molecular assays and animal models to map how the FAAH-OUT region affects gene expression and how that, in turn, shapes levels of anandamide and other lipids. Some reports published in 2023 and later described how the FAAH-OUT variant could “turn down” FAAH expression through epigenetic or transcriptional mechanisms, offering a plausible molecular model for Jo’s phenotype. These studies strengthened the link between her genotype and the observed physiology and suggested precise molecular levers for drug discovery.
Those follow-on studies also refined expectations. Whereas early coverage framed Jo as nearly immune to pain, subsequent work stressed nuance: her sensitivity is reduced, her anxiety is low, but she retains enough protective sensation to avoid the devastating injuries seen in other pain-insensitive conditions. The newer papers underscore a hopeful caution: Jo’s case is a proof of concept, not an off-the-shelf therapy.
Jo’s story raises ethical questions beyond the laboratory. If a drug could safely reproduce parts of her biology, who should receive it? Pain is both a scourge and a signal; removing it entirely carries risks. Would we use such medicine for acute surgical pain, for chronic neuropathic pain, or — more controversially — to reduce anxiety and reshape personality? These are not purely scientific choices. They involve social values, regulatory frameworks and questions about how much medical science should change the emotional texture of human life.
There is also the risk that rare case studies become exaggerated in public stories. Sensational headlines may sell papers but they can oversimplify. Jo’s lived reality is not a comic-book superpower. It is a combination of genetic variation and long-term adaptation. Any public conversation must respect that nuance and avoid promising miracles before safety and reproducibility are well established.
Funks Swabbie
