KNOW THYSELF
The signs of aging are obvious to most of us. Grey hair, aching joints, impairment of vision or hearing, and the dreaded week-long hangover after a night out all make it clear we are decaying at an ever-increasing rate. But while those things make us feel old, what’s actually happening in our body is a series of complex, interconnected processes. Over time, scientists have gotten a grip of these procedures and put them together to form the “hallmarks of aging.” To scientists, these hallmarks represent a chance to tackle the underlying cause of a great deal of disease and suffering. To immortalists, they may hold the key to a never-ending life.
The nine hallmarks, as they were called in a 2013 paper published in the journal Cell,[1] are not the easiest to understand. Regardless, I’ll list them here: epigenetic alterations, loss of proteostasis, deregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, altered intercellular communication, genomic instability, and telomere attrition. Most of those descriptions mean absolutely nothing to the layperson, but they are important enough to be worthy of further exploration.
First, it’s crucial to have a vague understanding of how our bodies work on a cellular level. The human genome, often spoken about but rarely understood, acts as what is commonly described as an “instruction book for the human body.” The genome is made up of a long sequence of DNA strands and contains all the information needed to build and maintain a human.[2] DNA strands are wound around spools of proteins called histones, and these are quite important. Histones and DNA have chemical handles, levers, and switches attached to them which allow certain genes to be turned on and off.[3] Skin cells and brain cells are vastly different from each other but are both made up of DNA. Their differences are created by the on/off buttons for the genes. Flip a switch here, turn a handle there, and you’ve got a completely different cell performing an entirely new task. The handles, levers, and cranks make up the epigenome, and this is crucial for the first hallmark of aging. As we age, the epigenome changes, and some of the levers are lost, added where they’re not needed, or moved around.[4] As you’d imagine, this causes havoc among cells and can even turn them cancerous.[5] Scientists discovered this hallmark by studying yeast, worms, and flies. This research found there is one particular group of proteins that influence the epigenome: sirtuins, which brought Sinclair global fame. In past trials, mice made deficient in one the seven mouse sirtuins showed signs of accelerated aging, while superabundant levels of the same sirtuin made them live longer. Interestingly, it’s not just age that affects the epigenome—diet, pharmaceutical, and lifestyle factors can all change those levers.[6]
So we know genes can be turned off and on by the epigenome, which can go haywire with age, but what do the genes do? Their primary job is to provide the information to make proteins, the heart of the cell’s biology that regulate almost all its chemical reactions and provide structure.[7] These proteins are folded into complex shapes like origami in order to perform their jobs. But as we age, our origami skills deteriorate; proteins are damaged, and they begin to misfold. When that happens, not only do they cease performing their jobs properly, they also clump together and become toxic. This clumping causes a host of problems, including Alzheimer’s disease. When these proteins are well-balanced and behaving properly, it’s called proteostasis. Cells have elaborate and complex systems designed to keep proteins in order, including specialized molecular devices that repair and refold them. Scientists established the key role proteostasis plays in aging by proving misfolded proteins increase with age and are found in the brain and muscle of Alzheimer’s patients. Researchers have also managed to extend the life of mice by enhancing protein quality control through gene alteration and drugs.[8]
The inner workings of a human cell contain the secrets of further hallmarks of aging. Mitochondria, often called the powerhouses of the cell, produce energy. But they also create free radicals, known as Reactive Oxygen Species (ROS), that damage nearly every molecule they come into contact with. For a long time scientists saw mitochondria as the main culprit behind the aging process and sought ways to eliminate them from the body. But more recently the scientific consensus about this has been challenged. Studies are now suggesting that reducing ROS has little impact on health. In fact, increasing ROS may be beneficial. The latest thinking suggests that ROS send signals to the body warning that cells are under stress, and this could kick regenerative functions into gear; perhaps ROS production needs to be kept in a “Goldilocks” range—not too much, not too little.[9]
The average human cell contains the string of three billion DNA letters that make up the genome. If the genome is faulty for whatever reason, your body may not run so smoothly. Past research has estimated that the DNA in each cell is damaged up to one million times per day by external factors like radiation or pollution and internal sources like oxygen-free radicals. And while our DNA does have processes in place to detect and repair that damage, as we age the repairs become increasingly imperfect, and problems with the genome begin to build up, which eventually can cause cancer. In both humans and mice, compromised DNA repair has been linked with accelerated aging.
The fifth hallmark of aging refers to a set of very basic rules that govern all animals. When nutrients are in abundance, animals—including humans—grow and reproduce. When the supply of nutrients becomes limited, evolution has taught our bodies to focus on maintenance and repair. Studies suggest if we were able to trick the body into thinking nutrients were scarce—with drugs like rapamycin, or simply starving ourselves—the body’s cells would focus on regeneration and potentially slow the aging process. This has been partially proven in mice and other species, and is one of the most important hallmarks for immortalists looking for ways to increase their lifespan. Neal VanDeRee’s intermittent fasting is an attempt to tap into this.
The next hallmark involves a controversial topic covered in more detail in a later chapter: stem cells. Our bodies have a powerful ability to regenerate and heal themselves, and that process is almost completely reliant on our stem cells, the source of new cells in virtually every tissue in the human body. When stem cells are needed, they replicate, but that ability to divide declines with age, meaning we can lose our regenerative powers as we get older.
So far, each hallmark has focused on the processes that lead to the disrepair of our cells. But communication between the cells and tissue is also a crucial factor in maintaining health as we age. Communication occurs through a number of methods, including through hormones, but can be blocked by inflammation in the body. When we’re still young, inflammation is usually a response to an injury and eases as the body heals. But as we age, a low level of constant inflammation can appear, unrelated to injuries. This type of inflammation isn’t just uncomfortable and potentially debilitating, it’s also damaging to the surrounding tissue. One way of easing chronic age-related inflammation could be to improve communication between the cells. The young blood transfusions which have made Silicon Valley look so weird are often touted as one potential solution to the inflammation problem.
Telomeres are often brought up by immortalists and longevity advocates as one of the secrets to extending life. They have three main uses that we know of. At the end of each strand of DNA, telomeres act as a protective cap. In the past they’ve been compared to aglets, the plastic tips at the end of shoelaces that stop them getting frayed. They also help organize each of the forty-six chromosomes within the nucleus, the control center of cells. Finally, they allow the chromosome to be replicated correctly during cell division. Every time a cell divides, telomeres become shorter, and eventually when they become too short the cell takes action. This usually triggers the cell to die but can sometimes make them dangerous. Research in mice has shown that when the telomerase enzyme is reduced, the mice show signs of premature aging, and when their telomeres are given a boost, their lifespan is extended. However, the role of telomeres in human aging is still unclear. Some believe the length of telomeres is a good predictor of lifespan, but others think it is responsible for the signs of aging, like greying hair, rather than the aging itself.
The final hallmark of aging concerns the mortality of the cells themselves. When they reach the point where they can no longer replicate, they are considered senescent cells. Instead of dying or disappearing, the cells hang around secreting molecules into their surrounding area. As we age, these senescent cells accumulate. For a long time, it was debated among the scientific community whether senescent cells made us age faster or if they were some kind of protection against the development of cancer. More recently, research in genetically engineered mice showed that if senescent cells were removed, there were clear health benefits, including longer life.
The hallmarks of aging have become something of a constant in aging research. But some major players in the field don’t see them as complete. Steven Austad is a senior scientific director at the American Federation for Aging Research, a co-director at the University of Alabama’s Nathan Shock Center of Excellence in the Basic Biology of Aging, and a Distinguished Professor in the Department of Biology—all of which suggest he knows a thing or two about aging. He told me there is nothing new or novel about the hallmarks, but they do act as a benchmark against which to compare new research, even if they may not be complete. “I know of at least three different people now who are writing about updating those. But I think, in terms of summarizing what we know about what goes wrong with aging, they’re okay. They’re a little bit redundant, they overlap. Some of them are processes, some of them are things. But it’s reached a point in the field where everybody has to nod to the hallmarks before they do much else,” Austad said on a call.
Like this book, Austad’s journey into aging featured an early encounter with an opossum. He initially trained in evolutionary ecology and was conducting field research with the animals when he came upon a curious discovery—they age incredibly rapidly. By the time an opossum reaches nineteen months to two years old, it is already approaching the end of its life, assuming it hasn’t been flattened by a car in a sad Florida suburb. This short lifespan is tiny in comparison to that of a house cat, which is a similar size but lives much longer. The plight of the opossum encouraged Austad to study aging. He was particularly interested in the evolutionary question of why we age, but he never thought his chosen field of study would attract the attention of those who believe they can be immortal. “I was probably in the field for ten or fifteen years before it ever occurred to me that humans would have interest in this because they wanted to live longer,” he said.
Austad is upbeat about the progress made in the field of aging. In 2000 he was quoted in a Scientific American article saying the first 150-year-old person “is probably alive right now.” A fellow expert on aging, Jay Olshansky, disagreed, and the two made a wager. In September that year, they put $150 each into an investment contract and agreed that the money and any returns would be paid out to the winner or his descendants in 2150. Austad will win the bet if a human has lived until 150 and maintained their mental functions when they reached that milestone.[10] The venture received national attention, and Austad was even contacted by a man who had seen the news and wanted to make a wager of his own with the expert—that he would live longer than Jeanne Calment, the oldest documented human, who died at age 122. Austad said he was tempted to take the money but realized he didn’t want to be rooting for someone to die. Incidents like this, however, made him appreciate the passion of those who believe in immortality.
Now, like other researchers in his field, Austad fights a strange battle. He sees there is genuine promise in the science aiming to address the nine hallmarks, and remarkable progress is being made at a breakneck speed right now, but there’s still a concerning pattern of people taking any small breakthrough and describing it as the secret to eternal life. “I think there’s some real promise. Not for living forever, of course, not for immortality. But for prolonging health I think there’s some real promise in the area, but people have taken it to ridiculous extremes,” he told me. “You’re constantly fighting this rearguard action against this type of claim, while at the same time trying to point out that there is legitimate research with legitimate promise. And just by debunking these extreme claims doesn’t mean you’re debunking the whole idea that you can improve health and extend health. It’s a balancing act.”
One of the more promising areas of research has come from the final hallmark listed above, the senescence of cells. Senolytics was one of the first scientific areas to attract attention—and dollars—from technology investors. Over time, evidence accrued that senescent cells, the cells which have ceased to divide and then hang around causing mischief, are a key factor in the aging process and a potential cause for some of the deadliest diseases linked with aging. They are also known, however, to form some kind of protection against tumors forming in the body. Now, a race has begun to develop drugs capable of eliminating either the right type or the correct amount of senescent cells in order to prevent certain diseases or reduce the impact of aging, potentially lengthening the lifespan of humans in the process. A number of scientists have made significant progress in the area of senescence, none more so than Dr. Judith Campisi.
Campisi took an unconventional route to the aging industry. After attending an all-girls Catholic high school in New York City, she had no idea what to do next. Nobody in her family attended college and money was tight, but she enrolled in a local college despite not knowing what to study. Each of the course descriptions in the college paraphernalia showed the percentage of males and females in each class. Campisi chose chemistry, one of the classes with the most boys. She later said although she knew she was good at the subject, her main motivation was “teenage hormones.” At the end of her two-year program, she went through several jobs in several fields, including pharmaceuticals, working as an editorial assistant at a small newspaper, and pumping gas. None of them stuck, so she took an extended road trip with a friend. Around that time, she decided to go back to school to pursue chemistry further. Campisi completed a four-year degree first, then went straight to graduate school, and later earned a PhD from the State University of New York at Stony Brook. This was followed by a postdoctoral fellowship at the Dana-Farber Cancer Institute in Boston, where she worked in the lab of Arthur Pardee, a renowned expert on the cell cycle.
Campisi jumped headlong into cancer research, a field she knew little about. When she secured her first faculty position in 1984 at Boston University Medical School, she took the advice of her mentor Pardee and picked a project well away from the mainstream. Oncogenes had recently been discovered as a key driving factor behind cancer, and everyone was rushing to start research into the topic. But with a small lab and a crowded field, Campisi decided to study why we don’t get cancer, or tumor suppression. She believed this path would be less competitive and allow her to make more of an impact in the science community, a belief that was proven correct. The study of tumor suppression also led her to the field of aging.[11]
Many of the diseases caused by aging, such as heart disease, kidney failure, and neurodegeneration, all involve the gradual degradation of the body, where age takes hold and organs begin to fail over time. But there is one disease that doesn’t follow that pattern. Cancer involves extreme mutation of the cells brought on by damage to the DNA. Once a cell is cancerous, it can mutate in hundreds of different ways to avoid the body’s processes that would either repair it or force it to die permanently. As one of the ways to guard against cancer, the body shuts down cells which have ceased to divide and are open to damage—the senescent cells mentioned in the hallmarks of aging.
Researchers initially believed these senescent cells were crucial in the body’s fight to suppress tumors, but Campisi discovered they were also damaging the tissue around them, contributing to aging. In 1996–1997, two editors from Cell and the Journal of the American Geriatrics Society asked her to write papers on this theory of aging. It took five years to prove how the theory works in a mouse. Campisi’s study appeared in the Proceedings of the National Academy of Sciences of the United States of America, and in 2008, her team described the secretion, called SASP—the Senescence-Associated Secretory Phenotype—in PloS Biology. That later paper became one of the most cited in biomedical research.[12]
From there, a whole new area of biotechnology was born, where companies raced to create the first drug to selectively eliminate senescent cells. “I’m very optimistic about senolytic drugs,” Campisi told me on a call. “There are still big gaps in our knowledge, big, big gaps in our knowledge, but I think they are on the horizon, they’re being developed, and they will be used. But these are not immortality drugs.”
When her research shifted into aging, she began to notice the frenzy around any related studies, and the tendency of some groups to link everything to immortality. When I spoke to Campisi about her experience with immortality-seekers, she was patient, informative, and utterly exhausted by people claiming we can live forever. “When Larry Page first started Calico, he declared that the mission of Calico was to defeat death. I said, ‘What?’ As long as I’ve been working in aging, not so much senescence but aging, I realized that there are first of all people who confuse aging and death, and secondly there are people who really believe that physical immortality is real and a possibility,” Campisi said.
The confusion between the study of aging and the halting of death has been going on for decades, according to Campisi. The idea of cells dividing indefinitely and organismal immortality stretches back to early in the twentieth century, when French biologist Alexis Carrel, a transplantation surgeon who won a Nobel Prize for his work in that area, announced a discovery from his work with in-culture chick embryos. He noticed the cells appeared to divide indefinitely when in this state, and he wrote a paper proposing that organismal mortality was linked with multicellularity. He thought if we could understand why the chick embryo cells divide indefinitely, we might discover why organisms are mortal.[13] “If you think about it, what was this guy thinking about?” asked Campisi. “If you dump hydrochloric acid on these cells, I guarantee you they’re going to die. And so it was this confusion between replicative capacity and organismal mortality.”
And the confusion didn’t stop there. Leonard Hayflick, an American anatomist, faced an uphill battle to convince the world Carrel was wrong. In 1962 at the Wistar Institute in Philadelphia, Pennsylvania, Hayflick demonstrated that a regular human fetal cell population divides between forty and sixty times before entering a senescent state, directly contradicting Carrel’s assertion that cells are immortal.[14] Hayflick also noticed the same did not apply to cancer cells, which did seem to multiply forever if left unchecked. He was the first person to suggest that senescent cells were perhaps associated with anti-cancer measures, and he turned out to be correct. He also linked that mechanism with aging—“based on nothing,” according to Campisi—and again was found to be right.
Campisi is quick to urge caution with senolytics and says the drugs still have a long way to go. A lot of research right now is focused on how to make them more selective, and there has been promising research with mice. “We made a transgenic mouse in which we can eliminate senescent cells at any point in the lifespan. Then you cross those mice to disease prone mice, and you can show that eliminating senescent cells either delays the onset or lessens the symptoms or in a few cases even reverses a surprisingly large number of age-related pathologies. But the mice still die, and they still die pretty much on time,” Campisi explained.
By altering the genes of these mice, Campisi’s lab has mimicked what senolytic drugs are expected to do—to kill senescent cells at any point in the lifespan of a human. But killing the cells isn’t the only way to attack the problem. Senescent cells drive so many age-related diseases not because they simply exist, but because of their secretion of molecules. This secretion finds its way into the tissue and causes low-level chronic inflammation. Senomorphic drugs have the potential to halt this secretion, and are encouragingly made of natural compounds. This gives scientists like Campisi the hope that the issue can ultimately be addressed with supplements and dietary intervention rather than the Big Pharma–produced senolytic drugs.
Campisi’s work has led to the private sector startups de Grey puts so much faith in. She cofounded Unity Biotechnology in 2011 with the specific aim of developing senolytic drugs. The company immediately attracted investors from Silicon Valley’s wealthiest, raising over $200 million from the likes of Bezos, Thiel, and notable venture capitalists.[15] Unity went public in 2018, raising $85 million through its Nasdaq listing at a market capitalization of $700 million.[16] But in August 2020, the company’s shares dropped 60 percent. A clinical trial involving the lead drug candidate, intended for patients with osteoarthritis, produced disappointing results. Unity also cut 30 percent of its employees.[17]
Campisi added two major caveats to the progress of her research. The first was that no matter what, it remained highly unlikely any of the results would drastically extend the human lifespan. She believes humans have a maximum lifespan of around 115, give or take ten years, although she’s prepared to be proved wrong. “Now, does that mean ten years from now or one hundred years from now we won’t find a way to break through that barrier? I can’t say no forever. We’re not soothsayers,” she said. “But based on our current knowledge, it’s extremely unlikely. I usually follow this up and say even though I consider myself a good scientist—I never say never and never say always—I can guarantee one thing: you will die one day.”
Campisi’s area of expertise inevitably brought her into the same orbit as de Grey. The SENS Foundation funded some of Campisi’s work at the Buck Institute. She has known him for years and sits on the SENS Research Advisory Board.[18] She told me de Grey wears two hats—one for the public and investors, where he makes outlandish claims about living for thousands of years, and the other for the scientists he supports. “When I talk to Aubrey about that work, he’s rational. He doesn’t know as much, he’s not a trained scientist…but he’s quite rational,” she said. “He puts these hats on depending upon his audience. What does he really believe? I don’t know, I’ve never gotten him drunk enough.”
Despite Campisi’s pleas, immortalists still see senolytics as one of the most promising areas of research that could address one of the major hallmarks of aging. But it’s still hard to stop death if you can’t see it coming. If immortalists are to reach escape velocity and live forever, they need to have a good understanding of their current health and how many years they might have left. Knowing your chronological age is really helpful for throwing birthday parties and applying for a passport, but in the world of the immortalists, only your biological age matters.
Theoretically, an accurate biological age would tell you roughly how much longer you will survive, or at least how many good years you might have left. Unnatural deaths can’t be foreseen, of course, but most people who live comfortably will die of old age, even if that’s not what is written on their death certificate. Prior to the COVID-19 pandemic, around one in four deaths in the United States were due to heart disease; that’s 659,041 people in 2019.[19] Cancer was just as lethal, accounting for 599,601 deaths the same year.[20] But research as far back as 1990 suggests that even if we were to cure cancer, heart disease, and diabetes, only a handful of years would be added to the lifespan of the average American’s life.[21] When a person’s body ages to a certain point, the general decay makes ideal circumstances for these kinds of diseases to emerge, so even if cancer were beaten, the problem of aging remains. Put more simply, when your body reaches a certain biological age, it’s just a matter of what’s going to kill you, not if something is going to kill you.
Forecasting that point of no return is difficult. Through the study of epigenetics—the small indicators of aging on the cellular level—scientists have developed a clock which can supposedly tell a person’s biological age. The epigenetic clock takes data from the epigenome to predict how far along your body is in the aging process. The first such clock was developed in 2011 by Steve Horvath, a biostatistician at the University of California, Los Angeles, after he analyzed hundreds of epigenetic markers.[22] The process involved measuring the specific patterns which are linked to aging and disease and comparing the results against what would be expected for a person of the same age as the participant. At the end, a person is told whether they are aging faster or slower than expected, and by roughly how many years.
Horvath initially had a tough time getting his results published amid skepticism over his claims. [23] But once the science was widely recognized, a handful of companies began selling kits and services based on Horvath’s clock. Customers typically pay around $500 to send saliva or blood to a lab and receive results explaining how old their body is.
This may seem like a vital tool for an immortalist looking to reach escape velocity, but some doubts remain. Although the kits are based on the same science as Horvath’s, they are completely unregulated by the FDA and aren’t independently evaluated. The tests are not accurate predictions of how long someone will live, and anyone paying for them would surely know that. For one thing, we don’t know what kind of accident or illness is ready to jump out on us, and secondly, the technology is not that accurate. So it’s not immediately clear what an immortalist would gain from the average epigenetic clock. Unlike genetic testing, the results don’t tell a person what their chances of developing a certain disease is. All they are told is how much older or younger their bodies are than other people their age.
Even if a person is older than expected, the solution almost all of the time is to eat healthier, sleep better, and exercise. It doesn’t take $500 to realize that will help everyone, regardless of their biological age. Epigenetic clocks are not just a potentially massive waste of money, there are other more nefarious and dystopian uses of them that would impact society. Some of these clockmakers have attempted to sell them to insurance firms, offering them the means to roughly gauge how old their customers’ bodies are before deciding on their premium costs. They also represent an opportunity for mass data collection, and employers could even use them to ensure prospective new employees were suitably healthy to become an effective long-term hire.[24]
Some experts have raised significant doubts over the validity of the epigenetic clock concept. Leonard Schalkwyk, Professor of Human Genetics at the University of Essex in England, and Jonathan Mill, Professor of Epigenetics at the University of Exeter, wrote an article in 2020[25] comparing data gleaned from epigenetic clock models against their own DNA methylation results. They found that epigenetic age doesn’t move at a steady pace and performs differently depending on which tissue is examined.
They argued that our epigenetic aging slows as we get older, particularly as we enter old age. “Ultimately, our work shows that researchers need to be careful when using the epigenetic clock to estimate how old people are. Age acceleration really does appear to be age dependent, and care should be taken when interpreting any age acceleration associations,” the pair wrote. “The epigenetic clock is a useful tool for researchers, but given the limited nature of the DNA methylation profile that the clock is based on, taking it at face value could lead to misleading results.”[26]
Austad was also dismissive of any test that claims to tell someone their biological age. “There are many ways that people are saying they can do this. Some of them are frankly bogus, and some of them have some promise. But there is an assumption underlying all of this, not very well validated, which is that you have a biological age, rather than your heart has a biological age and your kidney may have another biological age and your brain may have another biological age. So there’s some interesting work going on in that area, but I don’t think I would say anyone should take these biological age metrics on a personal level all that seriously,” he said.
Epigenetic clocks are just one method claiming to determine the speed of a person’s aging process. A number of companies offer blood work and testing which list biomarkers—most of which are linked to the nine hallmarks of aging—so customers can plot their best approach to slowing or even reversing aging. Among those offering this service is the Life Extension Foundation, a company run by Bill Faloon, one of the founders of the Church of Perpetual Life. On the company’s website, one of the main sections is Lab Testing, where well over one hundred different types of tests are listed.
“Are You Healthy? These Tests Reveal the Truth,” reads the banner across the top of the page. Rudi Hoffman, the cryonics insurance salesman, is one of their customers. On one of the days I called him, he had just completed one of his blood tests, where he sends off a vial of blood and gets back five or six pages of biomarkers. He is then able to call the Life Extension Foundation and have a health consultant go through the results with him to explain where he’s going wrong and what he needs to do to stay healthy for longer. Fortunately, the solution to any of the deficiencies found in the test are located on the very same website—in the hundreds of vitamins and supplements on sale there.
It’s a familiar story. The private sector moved in on the telomere craze in the mid-2010s, offering tests to those seeking to understand the length of the protective caps on the end of their DNA strands. Telomere Diagnostics, a company founded in Menlo Park, California, began offering $89 tests to determine the length of telomeres in 2016. Customers mailed in a drop of blood and received a calculation of their age in “TeloYears,” which worked in much the same way as epigenetic tests. For a little extra, users could also sign up to receive advice from an expert on improving diet, sleep, and stress levels in the hopes their telomeres would lengthen. But experts in the telomere field were far from convinced.
Mary Armanios, MD, of the Telomere Center in the McKusick-Nathans Institute of Genetic Medicine at Johns Hopkins University School of Medicine wrote a paper in 2018 titled “Telomeres in the Clinic, Not on the TV” which cast severe doubt on the legitimacy of the tests offered by private companies.[27] She argued the products present an oversimplified view of telomere length health by saying short telomeres are bad and long telomeres are a sign of youthfulness. Armanios called into question the quality of the testing, saying the assays used to measure telomere length in direct-to-consumer tests have been found to be “highly variable” and wanting when it came to “reproducibility and robustness.” She also pointed to problems with interpretation, as many of the private company tests only consider the median value as normal, which means anything even slightly shorter than that is considered an aged telomere level, and anything longer is youthful. Telomere length in the human population is more nuanced than this, Armanios argues. “The direct-to-consumer telomere testing thus risks causing unnecessary anxiety, with some believing they are ‘biologically aged’ and further leading them to pursue untested products,” her paper stated.
As if this weren’t bad enough, the tests and their interpretation do not consider the growing body of evidence suggesting long telomere length is not linked to youthfulness, but to a risk of several forms of cancers. The conclusion of the paper is damning: “Recognizing the clinical indications in which telomere length testing matters for patient care decisions exemplifies molecular medicine at its best. Distinguishing these indications from commercial testing is critical. While the former may be lifesaving, the latter may be considered a form of molecular palm reading.” (Telomere Diagnostics switched its entire focus when the pandemic hit and abandoned its TeloYears products, instead using its laboratories to offer coronavirus testing.)
Despite pushback from the scientific community, new devices and tests constantly appear. The AgeMeter is a nonintrusive method of tracking physiological biomarkers for aging. It looks a little like a chunky iPad and tests for numerous signs that a person is getting older, like memory, reaction time, hearing, agility, decision speed, and lung function. The device is mostly marketed to health care providers, but is available for individuals to buy at the modest price of $2,500. The AgeMeter website features a testimonial from noted geneticist George Church and a fairly vague quote from David Sinclair explaining the need for such a device. It is far more straightforward than epigenetic clock offerings, but it’s easy to see how it appeals to the neurosis of those concerned with aging.
As de Grey told me in the previous chapter, the earlier products offering immortality were easily identifiable as fakes, but those on the fringes of life extension are more ambiguous. It’s a trend seen in this area of science in general, according to Austad. He told me that twenty years ago there was a very sharp distinction between what was completely bogus and what was genuine, but now that line has blurred. “I have people all the time asking me who can I get to prescribe for me some drug that they read about in the press,” he said. “It puts me in an awkward position because I don’t want to say there’s no science behind that. But I can say there’s no science that suggests that humans are ready to try these things yet.”
Try telling an immortalist that.