Sharon Moalem’s primary goal in Survival of the Sickest is to explore the evolutionary history behind certain illnesses, diseases, and genetic disorders. Many of the chapters center around the question of why, if these diseases and disorders are harmful, evolution has not simply selected for individuals who do not have them. Moalem uses the book to illustrate how many inherited conditions still exist because they historically helped fight against more dangerous and life-threatening conditions. Thus, Moalem argues that evolution sometimes selected for traits that helped people survive in the short term and allowed them to reproduce and pass on those traits—even if, in the long term, those inherited conditions might end up being deadly.
Being able to survive deadly diseases in the short term is a necessary tradeoff to having a condition that might eventually cause harm, because those conditions allow enough time for humans to reproduce and pass on those inherited traits. Moalem’s first example of a disease that once provided short-term benefits is called hemochromatosis, a condition that causes iron to build up in the body. Hemochromatosis is inherited, particularly in people of Western European descent; if unchecked, it can lead to liver failure, heart failure, diabetes, arthritis, and cancer. However, in those with hemochromatosis, iron doesn’t build up in white blood cells called macrophages, which fight disease. In people without hemochromatosis, infectious agents feed on the iron in our macrophages, which actually makes the infectious agents more deadly. Thus, when the Bubonic Plague began in 1347, people who had hemochromatosis were more likely to survive it, because the bacteria were unable to access their iron and grow stronger. Thus, people who have inherited the gene for hemochromatosis may have done so because it allowed their ancestors to survive in the short term, even if it would harm them in the long term. There is a similar tradeoff with people who have a condition called favism, which is a condition that prevents people from clearing free radicals in their bloodstream. Free radicals are molecules or atoms with unpaired electrons that can wreak chemical havoc in cells in the body, and they often cause red blood cells to break down. This results in severe anemia, which can sometimes be deadly. However, Moalem posits that favism (which is found mostly in people around the Mediterranean) helps to combat malaria, because the parasitic protozoa that cause malaria can only infect normal, healthy red blood cells. Thus, those with favism, who do not have healthy red blood cells, are more likely to survive in their malaria-prevalent environments. So while anemia can be deadly, favism and the resulting anemia actually prevents people from dying from malaria and allows them to pass on those genes.
These genetic tradeoffs are not limited to safeguards against deadly diseases: in some cases, harmful adaptations have sprung up as a result of harsh nutritional conditions that existed thousands of years ago, which enabled people to survive even if it led to disease. Type 1 diabetes is thought to be an autoimmune disease wherein the body’s defense system mistakenly attacks the cells in the pancreas responsible for insulin production, and it is much more common in people of Northern European descent. For those with diabetes, the process through which insulin helps the body breaks down sugar doesn’t function properly, and the sugar in the blood builds up. Unmanaged, these abnormal blood sugar levels can lead to rapid dehydration, coma, and death. Though the theory is controversial, Moalem posits that flooding the bloodstream with sugar once acted as a kind of natural antifreeze that helped people survive in colder climates. Additionally, the extra sugar in the blood stream was not as problematic as it is today, because food and sugar were less available in general. During the Younger Dryas (a rapid period of climate change that occurred around 12,000 years ago, in which temperatures dropped significantly), people in Northern climates were particularly at risk of freezing—and those who were diabetic were more likely to survive because of their diabetes and the resulting sugar in their bloodstream. Thus, although diabetes is an unhelpful adaptation in the industrialized world, it was extremely helpful for primitive humans amid their harsh climate. Obesity may be another adaptation to harsh conditions. In 1987, British medical professor David Barker developed a theory that fetuses who experience poor nutrition develop “thrifty metabolisms that are much more efficient at hoarding energy.” Ten thousand years ago, the theory explains, this metabolism helped a baby survive when it was born into relative famine. But now, when a pregnant mother eats junk food, the embryo “receive[s] signals that it’s going to be born into a harsh environment where critical types of food are scarce.” As a result, when that baby is born and is surrounded by calorie-rich but nutritionally poor food, the “conservationist metabolism” that would once have helped the baby survive now leads to obesity.
In Moalem’s final example, he argues that everyone experiences these kinds of evolutionary tradeoffs, as even aging is an example of our bodies protecting us from something more deadly: cancer. Normally, our cells are only able to reproduce a specific number of times before genetic information begins to be lost. This prevents cells from becoming cancerous and reproducing an infinite number of times, unchecked. But as a result of these built-in controls, our cells gradually hit the limit of the number of times they can replicate, and our bodies begin to break down as a result. Thus, the aging process is the body’s way of protecting us from cancer in the short term, even if it causes significant damage later in life.
As the book’s title suggests, the common phrase “survival of the fittest” does not tell the whole story—Moalem illustrates in numerous examples how illness can sometimes be advantageous. In understanding why certain conditions developed and what they were fighting against, Moalem argues, humans can understand how to better treat those conditions without offsetting the advantages that the diseases proffered.
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Evolution and Illness ThemeTracker
Evolution and Illness Quotes in Survival of the Sickest
Then, in 1347, the plague begins its march across Europe. People who have the hemochromatosis mutation are especially resistant to infection because of their iron-starved macrophages. So, though it will kill them decades later, they are much more likely than people without hemochromatosis to survive the plague, reproduce, and pass the mutation on to their children. In a population where most people don’t survive until middle age, a genetic trait that will kill you when you get there but increases your chance of arriving is—well, something to ask for.
Today, we know that Aran suffered the effects of the most common genetic disorder in people of European descent—hemochromatosis, a disorder that may very well have helped his ancestors to survive the plague.
Today, Aran’s health has been restored through bloodletting, one of the oldest medical practices on earth.
Today, we understand much more about the complex interrelationship of our bodies, iron, infection, and conditions like hemochromatosis and anemia.
But what if a temporary diabetes-like condition occurred in a person who had significant brown fat living in an ice age environment? Food would probably be limited, so dietary blood-sugar load would already be low, and brown fat would convert most of that to heat, so the ice age “diabetic’s” blood sugar, even with less insulin, might never reach dangerous levels. Modern-day diabetics, on the other hand, with little or no brown fat, and little or no expo- sure to constant cold, have no use—and thus no outlet—for the sugar that accumulates in their blood.
By releasing free radicals and raising the level of oxidants, fava bean consumption makes the blood cells of non-G6PD deficient people a less hospitable place for malarial parasites. With all the free radicals, some red blood cells tend to break down. And when someone with a mild or partial deficiency in G6PD eats fava beans, the parasite is in deep trouble.
According to Villarreal, this capacity of African primates to support the persistent infection of other viruses may have put our evolution on “fast forward” by allowing more rapid mutation through exposure to other retroviruses. It’s possible that this capacity helped spur our evolution into humans.
According to the thrifty phenotype hypothesis, fetuses that experience poor nutrition develop “thrifty” metabolisms that are much more efficient at hoarding energy. When a baby with a thrifty phenotype was born 10,000 years ago during a time of relative famine, its conservationist metabolism helped it survive. When a baby with a thrifty metabolism is born in the twenty-first century surrounded by abundant food (that is also often nutritionally poor but calorie rich), it gets fat.
Many scientists believe cancer prevention is the “reason” cells have evolved with a limit on the number of times they can reproduce. The flip side to the Hayflick limit, of course—compromise, compromise—is aging. Once cells hit the limit, future reproductions don’t really work and things start to break down.
Biogenic obsolescence—that is to say, aging—might accomplish two similar ends. First, by clearing out older models, aging makes room for new models, which is exactly what creates the room for change—for evolution. Second, aging can protect the group by eliminating individuals that have become laden with parasites, preventing them from infecting the next generation. Sex and reproduction, in turn, are the way a species gets upgraded.
That still doesn’t explain the lack of evolutionary pressure against bipedalism and the accompanying reproductive risk caused by the change in pelvic shape. Unless—what if the water changed the equation somehow and made the process easier? If the water made the birthing process easier, then most of the evolutionary pressure would favor the advantages those aquatic apes gained from the shift to two feet.
I hope that you’ll come away from this book with an appreciation of three things. First, that life is in a constant state of creation. Evolution isn’t over—it’s all around you, changing as we go. Second, that nothing in our world exists in isolation. We—meaning humans and animals and plants and microbes and everything else—are all evolving together. And third, that our relationship with disease is often much more complex than we may have previously realized.
