Why wouldn't you do everything you can for your child?
In Christchurch, a two-year-old boy named Noah has begun taking Trikafta — the first medicine in history to treat the underlying cause of cystic fibrosis rather than merely its symptoms. His parents, who once contemplated leaving New Zealand entirely to secure him access, can now remain home after the drug was added to the country's funded medicines list. The story of one small child's birthday is also the story of what medicine, policy, and parental love can accomplish together — and of how profoundly a single decision can reshape the horizon of a life.
- Noah was diagnosed with cystic fibrosis at birth, setting his family on a path of two hours of daily medical care, strict dietary management, and constant vigilance against infection.
- As Trikafta transformed outcomes for CF patients overseas, his parents faced an agonising choice: uproot their lives to access the drug abroad, or wait and hope New Zealand would act.
- New Zealand's decision to expand Trikafta funding to children as young as two arrived in time — keeping the family in Christchurch and giving Noah access to a drug that could extend his life expectancy by 15 to 20 years.
- Trikafta does not cure cystic fibrosis, but it corrects the faulty protein at its root, promising thinner mucus, fewer infections, better nutrition absorption, and a fundamentally different future.
- International users of the drug — running marathons, living independently, starting families — now serve as living proof of what Noah's life might yet become.
Noah turned two in Christchurch last month, and his parents marked the occasion across three days of cake, cousins, and celebration. But the birthday carried an unusual weight: it coincided with the arrival of a drug that has rewritten what Eddie and Emily believe their son's future can hold.
Noah has cystic fibrosis, diagnosed within days of his birth after a routine scan led both parents to genetic testing. They discovered they were both carriers of the recessive mutation — a one-in-four chance their child would inherit it from both sides. Noah did. For Emily, then newly a mother, the diagnosis felt like a door closing on the healthy future she had imagined.
The years since have been defined by routine and vigilance. Every morning and evening brings nebuliser treatments and cupping sessions to clear mucus from Noah's lungs. Every meal requires carefully timed doses of creon, a pancreatic enzyme replacement, calibrated to the precise fat content of his food. Vitamins, monitoring, and a constant awareness of where germs gather have shaped the family's daily life. And yet Noah has thrived — sitting in the 98th percentile for weight, happy-go-lucky by his father's account, already lining up stuffed animals to watch Justin Bieber videos on his new microphone stand.
What changed everything was Trikafta — the first drug ever designed to treat the genetic root cause of cystic fibrosis rather than its symptoms. When it arrived on New Zealand's funded medicines list in 2023, it was available only to those six and older. Desperate, Eddie and Emily seriously considered relocating to England or Australia where younger children could already access it. Then New Zealand expanded the funding. They could stay.
For Noah, Trikafta should thin his mucus, reduce infections, improve his body's ability to absorb nutrients, and add an estimated 15 to 20 years to his life expectancy. It is not a cure — but it is, as his parents describe it, a transformation. What sustains them now are the stories filtering in from overseas: Trikafta users who have moved out of home, entered relationships, run marathons, and lived the ordinary extraordinary lives that most people take for granted. That is what they are hoping for Noah — not a miracle, but a life.
Noah turned two in Christchurch last month, and his parents threw him a three-day celebration. There was cake, presents, cousins running through the house. But this birthday carried weight that most second birthdays don't. For Eddie and Emily, the party was also a marker of something else: the arrival of a drug that has fundamentally altered what they believe their son's life can become.
Noah has cystic fibrosis. He was diagnosed within days of his birth, after a routine 20-week scan flagged something that sent both parents for genetic testing. They discovered they were both carriers of the recessive mutation—a 1 in 4 chance their child would inherit it from both of them. Noah did. The diagnosis arrived like a door closing, or so it felt at the time. Emily, now 30, remembers the shock of learning that the healthy baby she was carrying would face a lifelong battle against his own body's inability to process fats and proteins, and against the thick mucus that accumulates in his lungs, inviting infection.
For the first two years of Noah's life, his parents have spent roughly two hours every single day managing his care. Each morning and evening, nebuliser treatments and cupping sessions to loosen and drain the mucus from his lungs. Throughout the day, doses of creon—a pancreatic enzyme replacement—timed carefully with meals that contain precise amounts of fat. Vitamins. Monitoring. The mathematics of keeping a small body functioning. Emily, who works as a preschool teacher, describes the dietary management as their steepest learning curve. The creon has to be taken with food containing a specific amount of fat. Get it wrong and Noah's body won't absorb the nutrients he needs. They've learned to be cautious about where they take him—swimming pool changing rooms are off-limits, places where germs cluster. But they've also learned that Noah can still do most things. He can go places. He can have a life.
What changed was Trikafta. The drug arrived in New Zealand's funded medicines list in 2023, available to people six years and older. But Noah was only two. At one point, desperate to give their son access to what they knew could transform his future, Eddie and Emily seriously considered uprooting their lives—moving to England or Australia where the drug was already available. "Why wouldn't you do everything you can to get lifesaving medication for your child?" Emily asks. But then New Zealand came through. The funding expanded. They could stay in Christchurch, stay Cantabrians, and still give Noah access to the first drug ever designed to treat the underlying genetic cause of cystic fibrosis, not just its symptoms.
Trikafta works by correcting the faulty protein that CF creates. In Noah's case, it should thin his mucus, reducing infections and the scarring they cause. It should help his body absorb nutrients more efficiently. And it should do something almost unimaginable to parents who've spent two years in the trenches of daily medical care: it should add roughly 15 to 20 years to his life expectancy. That's not a cure. But it's a transformation.
Eddie, who manages a preschool himself, describes Noah as an "absolute champ" for the way he accepts his routine without complaint. The boy is happy-go-lucky, he says. He loves to sing—he got a microphone stand for his birthday and has been lining up his stuffed animals to watch Justin Bieber videos with him. He received a doctor's kit from his uncle and already knows what each instrument does, which Emily notes is unusual for a typical two-year-old. He's also in the 98th percentile for weight, thriving physically despite the condition that makes it so hard for his body to hold onto nutrition.
What keeps Emily and Eddie going now is the stories they've heard from people overseas who've been on Trikafta for longer. People who've moved out of home. People in relationships, having children. People running marathons and competing in Iron Man events. People living like normal kids, doing the things their friends do. That's what they hope for Noah. Not a cure, but a life. A real one.
Notable Quotes
We were ready to move to England or Australia to access this drug, but New Zealand came through and we can stay here and continue to be proud Cantabrians.— Eddie, Noah's father
We've heard stories about people on Trikafta overseas who are moving out of home, having relationships and kids, and even running marathons. That's what we hope for Noah—that one day he'll get to live like a normal Kiwi kid.— Emily, Noah's mother
The Hearth Conversation Another angle on the story
When you first learned Noah had cystic fibrosis, what was the thing you couldn't stop thinking about?
I think it was the weight of the routine. Two hours a day, every single day, for the rest of his life. That's not something you can take a break from. It's not like a broken arm that heals. It's the shape your entire family takes.
And then Trikafta became available. Did it feel like relief, or something more complicated?
Both. Relief, yes—but also a kind of grief lifting. They'd been ready to leave their home, their community, everything familiar, just to access this drug. When New Zealand funded it, it wasn't just about the medicine. It was about being able to stay.
Two hours a day is a lot. How do you keep that from consuming everything?
You find the moments where Noah is just a kid. He's obsessed with Justin Bieber. He lines up his teddies to watch videos. Those moments aren't separate from the medical care—they're woven through it. That's the actual life, not the routine around it.
What does 15 to 20 extra years mean to you as a parent?
It means he might get to choose his own life. Move out. Fall in love. Have children. Run a marathon if he wants to. Right now, we're managing his body. With Trikafta, maybe one day he gets to just live in it.
Do you think about the kids who don't have access to this drug?
Every day. We were almost one of them. We were packing to leave the country. The difference between Noah's future and another child's future shouldn't be geography.