Our relationship with iron is much more complex than it’s been considered traditionally. It’s essential—but it also provides a proverbial leg up to just about every biological threat to our lives. […] Parasites hunt us for our iron; cancer cells thrive on our iron. Finding, controlling, and using iron is the game of life. For bacteria, fungi, and protozoa, human blood and tissue are an iron gold mine. Add too much iron to the human system and you may just be loading up the buffet table.
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.
The Younger Dryas had arrived, and the world was changed.
Though humanity would survive, the short-term impact, especially for those populations that had moved north, was devastating. In less than a generation, virtually every learned method of survival—from the shelters they built to the hunting they practiced—was inadequate.
So when the grape dumps water at the first sign of frost, it’s actually protecting itself in two ways—first, by reducing water volume and second, by raising the sugar concentration of the water that remains. And that allows the grape to withstand colder temperature without freezing.
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.
There is one notable exception to Jablonski and Chaplin’s equation—and it’s the exception that proves the rule. The Inuit—the indigenous people of the subarctic—are dark-skinned, despite the limited sunlight of their home. If you think something fishy’s going on here, you’re right. But the reason they don’t need to evolve the lighter skin necessary to ensure sufficient vitamin D production is refreshingly simple. Their diet is full of fatty fish—which just happens to be one of the only foods in nature that is chock-full of vitamin D.
This made clean water a real challenge, and some theories suggest that different civilizations came up with different solutions. In Europe, they used fermentation—and the resulting alcohol killed microbes, even when, as was often the case, it was mixed with water. On the other side of the world, people purified their water by boiling it and making tea. As a result, there was evolutionary pressure in Europe to have the ability to drink, break down, and detoxify alcohol, while the pressure in Asia was a lot less.
Instead of worrying about whether or not there are distinct “races,” let's concentrate on what we do know and use that to advance medical science. What we do know is that distinct populations do share distinct genetic heritages, which are almost certainly the result of different evolutionary pressures our various ancestors experienced as they settled and resettled across the globe.
On the other hand, as much as plants want animals to eat their fruit, they don’t want animals to get much closer than that—when creatures start to nibble on their leaves or gnaw at their roots, things can get tricky. So plants have to be able to defend themselves. Just because they’re generally immobile doesn't mean they’re pushovers.
The next time you’re looking for some convenient birth control, you don’t have to snack on a field of clover, of course. But if you take many forms of the famous “Pill,” you’re not doing something all that different. The gifted chemist Carl Djerassi based his development of the Pill on just this kind of botanical birth control. He wasn’t using clover, though; he was using sweet potatoes—the Mexican yam to be exact.
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.
Former president Jimmy Carter has led a two-decade effort to spread understanding about the parasite’s method of reproduction to every corner of the world, ensuring that its victims avoid water when looking for relief and that its potential victims avoid water that could be infected. According to the Carter Center, the worldwide incidence of Guinea worm infections had dropped from 3.5 million in 1986 to just 10,674 in 2005.
Most of these microbes are found in the digestive system, where they play crucial roles. These intestinal bacteria, or gut flora, help to create energy by breaking down food products we otherwise couldn’t break down; they help to train our immune systems to identify and attack harmful organisms; they stimulate cell growth; and they even protect us against harmful bacteria.
Ewald believes that we can use this understanding to influence the evolution of parasites away from virulence. The basic theory is this—shut down the modes of transmission that don’t require human participation and suddenly all the evolutionary pressure is directed at allowing the human host to get up and get out.
By introducing the harmless virus to our bodies, we stimulate our immune systems to produce antibodies specifically tailored to defend against that virus. Then, if we are exposed to the harmful version, our bodies are prepared to defend themselves immediately.
McClintock believed that the jumps are a genomic response to internal or environmental stress that cells can't handle under their existing setup. Essentially, a challenge to survival triggers the organism to throw the mutation dice, hoping it will land on a change that will help. That’s what she thought was going on with the corn plants she was studying—too much heat or too little water triggered the corn to gamble its survival on finding a mutation that could help it survive.
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.
Essentially, one or more of the compounds in the vitamin supplements fed to the expectant mothers reached down into the mouse embryos and flicked the agouti gene into the “off” position. When the baby mice were born, their DNA still contained the agouti gene, but it wasn’t expressed—chemicals had attached to the gene and suppressed its instructions.
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.
Here’s the first thing we don’t know—we don’t have anywhere near a complete understanding of which genes are turned off or turned down by which methyl donors. For example, methylation of a gene that influences hair color might lead to a harmless change—but the same process that triggered methylation of the hair color gene may also be suppressing a tumor suppressor.
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.
