One is genetic diseases. Twenty years ago, about five thousand genetic diseases were known. Today it is seven thousand. The number of genetic diseases is constant. What has changed is our ability to identify them. Sometimes one rogue gene can cause a breakdown, as with Huntington’s disease, which used to be known as Huntington’s chorea, from the Greek for “dance,” a strange and decidedly insensitive reference to the jerky movements of Huntington’s sufferers. It is a thoroughly wretched disease, affecting about one person in every ten thousand. Symptoms usually first appear when the victim is in his or her thirties or forties, and progress ineluctably to senility and premature death. It is all because of one mutation in the HTT gene, which produces a protein called huntingtin, one of the largest and most complex proteins in the human body, and we have no idea what huntingtin is for.
Far more often, multiple genes are at play, usually in ways too complex to fully understand. The number of genes that have been implicated in inflammatory bowel disease, for instance, is comfortably over a hundred. At least forty have been linked to type 2 diabetes, and that is before you start to factor in other determinants like health and lifestyle. Most diseases have a complex array of triggers.
That means that it is often impossible to pinpoint a cause. Take multiple sclerosis, a disease of the central nervous system in which sufferers experience a gradual onset of paralysis and loss of motor control, nearly always beginning before the age of forty. It is indubitably genetic, but it also has a geographical element that no one can quite explain. People from northern Europe get it much more often than people from warmer climes. As David Bainbridge has observed, “Why a temperate climate should make you attack your own spinal cord is not so obvious. Yet the effect is clear, and it has even been shown that if you are a northerner you can reduce your risk by relocating southward before puberty.” It also affects women disproportionately, again for no reason that anyone has yet determined.
Mercifully, most genetic diseases are quite rare, often vanishingly so. One of the more famous sufferers of a rare genetic disorder was the artist Henri de Toulouse-Lautrec, who is thought to have suffered from pycnodysostosis. Toulouse-Lautrec was normally proportioned until puberty, but then his legs stopped growing while his trunk continued growing to normal adult size. In consequence, when standing, he looked as if he were on his knees. Only about two hundred cases of the disorder have ever been recorded.
Rare diseases are defined as diseases that afflict no more than one person in two thousand, and there is a paradox at their heart, which is that although each disease doesn’t affect many people, collectively they affect a lot. Altogether there are about seven thousand rare diseases—so many that about one person in seventeen in the developed world has one, which isn’t very rare at all. But, sadly, so long as a disease affects only a small number of people, it is unlikely to get much research attention. For 90 percent of rare diseases, there are no treatments at all.
A second category of disorders that have become more common in modern times, and represent a much greater risk for most of us, is what Professor Daniel Lieberman of Harvard calls mismatch diseases—that is, diseases brought on by our indolent and overindulgent modern lifestyles. The idea, roughly, is that we are born with the bodies of hunter-gatherers but pass our lives as couch potatoes. If we want to be healthy, we need to eat and move about a little more like our ancient ancestors did. That doesn’t mean we have to eat tubers and hunt wildebeest. It means we should consume a lot less processed and sugary foods and get more exercise. Failure to do that, however, is what is giving us the disorders like type 2 diabetes and cardiovascular disease that are killing us in great numbers. Indeed, as Lieberman notes, medical care is actually making things worse by treating the symptoms of mismatch diseases so effectively that we “unwittingly perpetuate their causes.” As Lieberman puts it with chilling bluntness, “You are most likely going to die from a mismatch disease.” Even more chillingly, he believes that 70 percent of the diseases that kill us could easily be preventable if we would just live more sensibly.
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When I met Washington University’s Michael Kinch in St. Louis, I asked him what he believed was the greatest disease risk to us now.
“Flu,” he said without hesitation. “Flu is way more dangerous than people think. For a start, it kills a lot of people already—about thirty to forty thousand every year in the United States—and that’s in a so-called good year. But it also evolves very rapidly, and that’s what makes it especially dangerous.”
Every February, the World Health Organization and the Centers for Disease Control get together and decide what to make the next flu vaccine from, usually based on what’s going on in eastern Asia. The problem is that flu strains are extremely variable and really hard to predict. You are probably aware that all flus have names like H5N1 or H3N2. That is because every flu virus has two types of proteins on its surface—hemagglutinin and neuraminidase—and these account for the H and N in their names. H5N1 means that the virus combines the fifth known iteration of hemagglutinin with the first known iteration of neuraminidase, and for some reason that is a particularly nasty combination. “H5N1 is the version commonly known as bird flu, and it kills between 50 to 90 percent of victims,” says Kinch. “Luckily, it isn’t readily transmissible between humans. So far this century, it has killed about four hundred people—roughly 60 percent of those it has infected. But look out if it mutates.”
Based on all the available information, the WHO and CDC announce their decision on February 28, and all the flu vaccine manufacturers in the world begin working on the same strain. Says Kinch, “From February to October they make the new flu vaccine, in the hope that we will be ready for the next big flu season. But when a really devastating new flu emerges, there’s no guarantee that we will actually have targeted the right virus.”
In the 2017–18 flu season, to take one recent example, people who had been vaccinated were only 36 percent less likely to get flu than those who hadn’t been vaccinated. In consequence, it was a bad year for flu in America, with a death toll estimated at eighty thousand. In the event of a really catastrophic epidemic—one that killed children or young adults in large numbers, say—Kinch believes we wouldn’t be able to produce vaccine fast enough to treat everyone, even if the vaccine was effective.
“The fact is,” he says, “we are really no better prepared for a bad outbreak today than we were when Spanish flu killed tens of millions of people a hundred years ago. The reason we haven’t had another experience like that isn’t because we have been especially vigilant. It’s because we have been lucky.”
*1 Because of the similarity of symptoms and difficulty of diagnosis, it is sometimes lumped in with chronic fatigue syndrome (CFS) but is really quite different. CFS (formally myalgic encephalomyelitis) tends to affect individuals, while epidemic neuromyasthenia hits populations.