There comes a point where we need to stop just pulling people out of the river. We need to go upstream and find out why they’re falling
Assuming that you’re not someone who engages in ultrarisky behaviors like BASE jumping, motorcycle racing, or texting and driving, the odds are overwhelming that you will die as a result of one of the chronic diseases of aging that I call the Four Horsemen: heart disease, cancer, neurodegenerative disease, or type 2 diabetes and related metabolic dysfunction. To achieve longevity—to live longer and live better for longer—we must understand and confront these causes of slow death.
Longevity has two components. The first is how long you live, your chronological lifespan, but the second and equally important part is how well you live—the quality of your years. This is called healthspan,
Death rates from cancer, on the other hand, have hardly budged in the more than fifty years since the War on Cancer was declared, despite hundreds of billions of dollars’ worth of public and private spending on research. Type 2 diabetes remains a raging public health crisis, showing no sign of abating, and Alzheimer’s disease and related neurodegenerative diseases stalk our growing elderly population, with virtually no effective treatments on the horizon.
Perhaps my biggest takeaway was that modern medicine does not really have a handle on when and how to treat the chronic diseases of aging that will likely kill most of us. This is in part because each of the Horsemen is intricately complex, more of a disease process than an acute illness like a common cold. The surprise is that this is actually good news for us, in a way. Each one of the Horsemen is cumulative, the product of multiple risk factors adding up and compounding over time. Many of these same individual risk factors, it turns out, are relatively easy to reduce or even eliminate.
One macronutrient, in particular, demands more of our attention than most people realize: not carbs, not fat, but protein becomes critically important as we age.
Exercise is by far the most potent longevity “drug.” No other intervention does nearly as much to prolong our lifespan and preserve our cognitive and physical function. But most people don’t do nearly enough—and exercising the wrong way can do as much harm as good.
What bothers me most about “First, do no harm,” though, is its implication that the best treatment option is always the one with the least immediate downside risk—and, very often, doing nothing at all.
Yet Medicine 2.0 has proved far less successful against long-term diseases such as cancer. While books like this always trumpet the fact that lifespans have nearly doubled since the late 1800s, the lion’s share of that progress may have resulted entirely from antibiotics and improved sanitation, as Steven Johnson points out in his book Extra Life. The Northwestern University economist Robert J. Gordon analyzed mortality data going back to 1900 (see figure 1) and found that if you subtract out deaths from the eight top infectious diseases, which were largely brought under control by the advent of antibiotics in the 1930s, overall mortality rates declined relatively little over the course of the twentieth century.
It is already obvious that medicine is changing rapidly in our era. Many pundits have been predicting a glorious new era of “personalized” or “precision” medicine, where our care will be tailored to our exact needs, down to our very genes. This is, obviously, a worthy goal; it is clear that no two patients are exactly alike, even when they are presenting with what appears to be an identical upper-respiratory illness.
Medicine 3.0 considers the patient as a unique individual. Medicine 2.0 treats everyone as basically the same, obeying the findings of the clinical trials that underlie evidence-based medicine. These trials take heterogeneous inputs (the people in the study or studies) and come up with homogeneous results (the average result across all those people). Evidence-based medicine then insists that we apply those average findings back to individuals. The problem is that no patient is strictly average. Medicine 3.0 takes the findings of evidence-based medicine and goes one step further, looking more deeply into the data to determine how our patient is similar or different from the “average” subject in the study, and how its findings might or might not be applicable to them. Think of it as “evidence-informed” medicine.
Another, related issue is that longevity itself, and healthspan in particular, doesn’t really fit into the business model of our current healthcare system. There are few insurance reimbursement codes for most of the largely preventive interventions that I believe are necessary to extend lifespan and healthspan. Health insurance companies won’t pay a doctor very much to tell a patient to change the way he eats, or to monitor his blood glucose levels in order to help prevent him from developing type 2 diabetes. Yet insurance will pay for this same patient’s (very expensive) insulin after he has been diagnosed.
The words “First, do no harm” do not appear in Hippocrates’s actual writings. He urged physicians to “practice two things in your dealings with disease: either help or do not harm the patient.” This was changed to “First, do no harm” by an aristocratic nineteenth-century British surgeon named Thomas Inman, whose other claim to fame was, well, nothing.
Our tactics in Medicine 3.0 fall into five broad domains: exercise, nutrition, sleep, emotional health, and exogenous molecules, meaning drugs, hormones, or supplements.
The data are unambiguous: exercise not only delays actual death but also prevents both cognitive and physical decline, better than any other intervention. We also tend to feel better when we exercise, so it probably has some harder-to-measure effect on emotional health as well.
According to research by Thomas Perls of Boston University and his colleagues, who run the New England Centenarian Study, one in five people in the general population will have received some type of cancer diagnosis by age seventy-two.
But when researchers did this, examining thousands of individuals via genome-wide association studies, they came up almost empty-handed. These individuals appeared to have very little in common with one another genetically. And their longevity may be due to dumb luck after all.