Willis sighed, and gestured around him at his office.
‘This has been my work for the past three years. Along with Werner syndrome, I’ve been studying the effects and causes of cellular senescence, seeking ways in which to delay the deleterious effects of human aging.’
‘Why?’ Lopez asked. ‘What’s the purpose exactly? Everybody dies eventually.’
‘Yes, they do,’ he agreed. ‘But the purpose of my work is to understand how we age and how to try to develop medicines that will ensure that people age comfortably, without the debilitating diseases that afflict the elderly. By studying things like cellular apoptosis — programmed cell death — it’s theoretically possible to reverse the process of aging.’
‘Surely that can’t work,’ Ethan said. ‘People have to age in order to die, and nothing is immortal.’
Tyler Willis smiled broadly.
‘In fact, that’s not entirely true. We see aging as a process that takes place across our own lifespans, and we see others age as we do. It’s something we’re used to, but in nature not every species ages at the same rate, and for some there is no aging process at all.’
Lopez raised an eyebrow.
‘You mean that some animals live forever?’
‘Perhaps not forever, but for long enough that to a human perspective they would appear immortal,’ Willis said. ‘The hydrozoan species Turritopsis nutricula is able to return from a mature adult to an immature polyp stage and back again, effectively meaning that it is considered biologically immortal and has no maximum lifespan. Colonies of sea anemones have been kept in laboratories for close to a century, can regenerate any body part and show no signs of aging. Some koi fish, a much larger and more complex species, have lived beyond two hundred years.’
‘That’s not quite the same as a mammal living for that long,’ Ethan pointed out.
‘But that’s my point,’ Tyler insisted, ‘delayed senescence isn’t species specific and can occur in mammals too. In May 2007, a fifty-tonne Bowhead whale caught off the coast of Alaska was found to have the head of an explosive harpoon embedded within its neck blubber. The four-inch arrow-shaped projectile had been manufactured in New Bedford, Massachusetts around 1890, making the whale a minimum of one hundred seventeen years old.’
‘A bit like Hiram Conley,’ Lopez said. ‘He had a Minie musket ball lodged in his right femur. According to analysis the wound was around one hundred forty years old.’
Tyler Willis grasped the edge of his desk.
‘You’re sure? You actually have evidence of this?’
‘It’s locked up,’ Lopez replied quickly, cursing inwardly at having revealed too much. ‘But our source is reliable. The main reason we’re here is to find out what the hell’s been going on with this Conley and how he could have ended up not just with that wound but with a fresh Minie ball in his shoulder.’
Willis seemed momentarily distracted, whispering to himself.
‘I’ll be damned, it’s true then.’ He looked at them. ‘Conley had been shot before I met him in the pass, before the ranger arrived. Somebody else shot him with a musket, maybe one of the others.’
‘When you were found,’ Ethan said, ‘you told Patrol Officer Zamora that Hiram Conley was too old to die, that you didn’t want him killed. You knew that he was very old then, didn’t you?’
Willis seemed to come back to the present. He looked at both Lopez and Ethan as though weighing them up, and then finally nodded.
‘I didn’t at first,’ he said simply.
‘What was wrong with him, exactly?’ Lopez asked.
Willis sighed heavily.
‘It’s very difficult to explain,’ he said. ‘You need to think differently about life and what it is before you can understand what happened to Hiram Conley. What you need to know is that nobody ever dies of old age, ever. What happens to us, and to all other species, is that the ability of our cells to divide without generating errors decreases the more times those cells are forced to divide. The gradual building up of cellular errors eventually results in programmed cell death, apoptosis, which leads to a specific cause of death such as organ failure, cancer and so on. We die as a result of illness brought on by age, but not by age itself.’
‘So technically people could live forever?’ Lopez asked, ‘if their cells could divide without errors.’
‘It’s possible,’ Willis nodded, ‘even as crazy as it sounds. But unfortunately it’s not quite as simple as that. Like everything else, aging is something that has evolved through natural selection. Most of the earliest forms of life on our planet were bacterial colonies and such like, forms which don’t necessarily suffer senescence because, as a colony, they survive for millions of years and continue the genetic heritage of the colony as a whole. However, with most forms of life aging has evolved because the longer something lives, the more likely it is to encounter a fatal incident, be it predation or an accident.’
‘We die just in case we have an accident?’ Lopez muttered. ‘Sounds like a bum deal.’
‘Not really,’ Willis said. ‘Evolution has resulted in a situation where it has become an advantage to have higher reproductive strategies at the youngest possible age, thus reducing the chances of some fatal event preventing reproduction and making a species extinct. Natural selection favors those species which can mate most effectively when they’re young and fit, and so the evolution of species has resulted in forms of life who mature early and mate young, before then growing old and passing away. There’s a resources issue too — if nothing ever died, then pretty soon all the planet’s resources would be consumed and nothing more could live. Each generation of species must thus make way for the next.’
‘So what was your angle on all of this?’ Lopez asked. ‘You were trying to eradicate age-related disease, but how?’
‘Disease generally comes about when people age,’ Tyler Willis said, ‘that much we know. What people don’t realize is that human diseases should have been eradicated by natural selection by now via inherited immunity or random mutation. The reason they haven’t been is therefore because humans mate young, and for most of our evolution have also died young. The presence of extensive age-related disease is a relatively new phenomenon because it’s only recently that people have reached their seventies and beyond on a regular basis. This means that natural selection only acts weakly against age-related disease because resilience to it hasn’t yet had the chance to evolve within us. My work involved studying how genetic manipulation might serve humanity by acting as a substitute for natural selection and creating specific genes resistant to such diseases, like Huntingdon’s or Alzheimer’s.’
‘Okay,’ Lopez said, ‘so how would you go about doing that?’
‘Well,’ Willis replied, ‘the main cause of aging in mammals is the degradation of telomeres in the nuclei of cells. Telomeres are like caps at the tips of chromosomes — you can think of them as fuel for the accurate division and replication of cells. As cells divide, telomeres become ever shorter, and eventually they are unable to support further cellular division without a build-up of errors or deleterious mutations, which cause the signs of aging such as muscle loss, degraded skin quality, organ failure and so on. If we can find a way of allowing cells to divide without losing the telomeres and building up those errors, we have a possible means of extending quality of life, if not longevity itself.’
‘Doesn’t sound so hard,’ Ethan said.
‘It’s hard,’ Willis assured him. ‘Mainly because the only kind of cells that naturally undergo this transformation into biologically immortal cells are those that cause cancer. The line between the two may be thin, but it’s the difference between curing someone and killing them.’