THREE

       THE BLIND EPIDEMIC

      IT WAS MAY 10, 2010, AND LONDON WAS ABUZZ. CHELSEA FOOTBALL CLUB HAD just won its fourth national championship by devastating Wigan Athletic, 8–0, on the final day of Premier League play. Meanwhile, Gordon Brown announced that he would be stepping down as prime minister in response to a disastrous parliamentary result for his Labour Party, which had lost more than ninety seats in the previous week’s general election.

      With the eyes of the English sports world on one part of London and the attention of the British political universe on another, the goings-on at Carlton House Terrace were missed by all but the most attentive observers of the president, council, and fellows of the Royal Society of London for Improving Natural Knowledge.

      More simply known as the Royal Society, the world’s oldest national scientific organization was established in 1660 to promote and disseminate “new science” by big thinkers of the day such as Sir Francis Bacon, the Enlightenment’s promulgator of “the prolongation of life.”¹ Befitting its rich scientific history, the society has held annual scientific events ever since. Highlights have included lectures by Sir Isaac Newton on gravity, Charles Babbage on his mechanical computer, and Sir Joseph Banks, who had just arrived back from Australia with a bounty of more than a thousand preserved plants that were all new to science.

      Even today, in a post-Enlightenment world, most of the events at the society are fascinating if not world changing. But the two-day meeting that commenced in the spring of 2010 was nothing short of that, for gathered together on that Monday and Tuesday was a motley group of researchers who were meeting to discuss an important “new science.”

      The gathering had been called by geneticist Dame Linda Partridge, bioanalytics pioneer Janet Thornton, and molecular neuroscientist Gillian Bates, all luminaries in their respective fields. The attendee list was no less impressive. Cynthia Kenyon spoke about her landmark work on a single mutation in the IGF-1 receptor gene that had doubled the lifespan of roundworms by activating DAF-16²—work that was first suggested by Partridge to be a worm-specific aberration³ but soon forced her and other leading researchers to confront long-held beliefs that aging could be controlled by a single gene. Thomas Nyström, from the University of Gothenburg, reported his discovery that Sir2 not only is important for genomic and epigenomic stability in yeast, it also prevents oxidized proteins from being passed on to young daughter cells.

      Brian Kennedy, a former Guarente student who was about to assume the presidency of the Buck Institute for Research on Aging, explained the ways in which genetic pathways that had been similarly conserved in a diverse array of species were likely to play similar roles in mammalian aging. Andrzej Bartke from Southern Illinois University, former PhD adviser to Michael “Marathon Mouse” Bonkowski, talked about how dwarf mice can live up to twice as long as normal mice, a record. Molecular biologist María Blasco explained how old mammalian cells are more likely than young cells to lose their identity and become cancerous. And geneticist Nir Barzilai spoke of genetic variants in long-lived humans and his belief that all aging-related diseases can be substantially prevented and human lives can be considerably extended with one relatively easy pharmaceutical intervention.

      Over the course of those two days, nineteen presenting scientists from some of the best research institutions in the world moved toward a provocative consensus and began to build a compelling case that would challenge conventional wisdom about human health and disease. Summarizing the meeting for the society later that fall, the biogerontologist David Gems would write that advances in our understanding of organismal senescence are all leading to a momentous singular conclusion: that aging is not an inevitable part of life but rather a “disease process with a broad spectrum of pathological consequences.”⁴ In this way of thinking, cancer, heart disease, Alzheimer’s, and other conditions we commonly associate with getting old are not necessarily diseases themselves but symptoms of something greater.

      Or, put more simply and perhaps even more seditiously: aging itself is a disease.

      THE LAW OF HUMAN MORTALITY

      If the idea that aging is a disease sounds strange to you, you’re not alone. Physicians and researchers have been avoiding saying that for a long time. Aging, we’ve long been told, is simply the process of growing old. And growing old has long been seen as an inevitable part of life.

      We see aging, after all, in nearly everything around us and, in particular, the things around us that look anything like us. The cows and pigs in our farms age. The dogs and cats in our homes do, too. The birds in the sky. The fish in the sea. The trees in the forest. The cells in our petri dishes. It always ends the same way: dust to dust.

      The connection between death and aging is so strong that the inevitability of the former governed the way we came to define the latter. When European societies first began keeping public death certificates in the 1600s, aging was a respected cause of death. Descriptions such as “decrepitude” or “feebleness due to old age” were commonly accepted explanations for death. But according to the seventeenth-century English demographer John Graunt, who wrote Natural and Political Observations Mentioned in a Following Index, and Made upon the Bills of Mortality, so were “fright,” “grief,” and “vomiting.”

      As we’ve moved forward in time, we’ve moved away from blaming death on old age. No one dies anymore from “getting old.” Over the past century, the Western medical community has come to believe not only that there is always a more immediate cause of death than aging but that it is imperative to identify that cause. In the past few decades, in fact, we’ve become rather fussy about this.

      The World Health Organization’s International Classification of Diseases, a list of illnesses, symptoms, and external causes of injury, was launched in 1893 with 161 headings. Today there are more than 14,000, and in most places where records of death are kept, doctors and public health officials use these codes to record both immediate and underlying causes of disability and death.⁵ That, in turn, helps medical leaders and policy makers around the globe make public health decisions. Broadly speaking, the more often a cause shows up on a death certificate, the more attention society gives to fighting it. This is why heart disease, type 2 diabetes, and dementia are major focuses of research and interventionary medical care, while aging is not, even though aging is the greatest cause of all those diseases.

      Age is sometimes considered an underlying factor at the end of someone’s life, but doctors never cite it as an immediate reason for death. Those who do run the risk of raising the ire of bureaucrats, who are prone to send the certificate back to the doctor for further information. Even worse, they are likely to endure the ridicule of their peers. David Gems, the deputy director of the Institute of Healthy Ageing at University College London and the same man who wrote the report from the Royal Society meeting on “the new science of aging,” told Medical Daily in 2015 that “the idea that people die of pure aging, without pathology, is nuts.”⁶

      But this misses the point. Separating aging from disease obfuscates a truth about how we reach the ends of our lives: though it’s certainly important to know why someone fell from a cliff, it’s equally important to know what brought that person to the precipice in the first place.

      Aging brings us to the precipice. Give any of us 100 years or so, and it brings us all there.

      In 1825, the British actuary Benjamin Gompertz, a learned member of the Royal Society, tried to explain this upward limit with a “Law of Human Mortality,” essentially a mathematical description of aging. He wrote, “It is possible that death may be the consequence of two generally co-existing causes; the one, chance, without previous disposition to death or deterioration; the other, a deterioration, or an increased