(Author’s Note: The following review was solicited and is written in accordance with this site’s policy for such reviews.)
Summary: A fast-paced, entertaining, informative account of how past evolution has shaped our current living conditions. Recommended – but with one major caveat.
One of the most common misconceptions about evolution is that it is a steady climb towards perfection, working over time to remove every defect. In fact, natural selection is not a skilled artisan but, to use Richard Dawkins’ phrase, a blind watchmaker. Evolution is a process of tinkering, of incremental change, and of modification of old structures to suit new purposes. Sometimes this can lead to a cul-de-sac of adaptation, where a certain trait or structure is globally suboptimal but locally optimal: it is provably inferior at what it does, and yet natural selection blocks improvement because any change would have to begin by temporarily making things even worse. Evolutionary legacies such as the vestigial appendix, the backwards human retina, and other genetic anachronisms give testament to the way such tradeoffs have shaped our species’ past.
Survival of the Sickest expands on this basic theme to argue for the influence of disease on humanity’s evolution, both inherited disorders and external pathogens. Dr. Moalem’s thesis will probably be familiar to most scientists and informed laypeople, but may come as a shock to the average reader: in some cases, evolution may actually favor the emergence of downright harmful traits and genetic diseases. If a gene variant keeps its possessors healthy and strong in the prime of life and helps them to leave more descendants, but ruthlessly cuts down those same people after they have passed their reproductive ages, there are circumstances under which it will be spread by natural selection. Even mutations that are outright harmful can be selected for, if they offer protection against an even more destructive scourge.
As anyone who’s debated evolution will probably know, the prime example is the gene that produces sickle-shaped red blood cells. When a person has two copies of this gene, it causes the debilitating ailment of sickle-cell anemia. But a person with one copy of this gene enjoys partial protection against malaria, a devastating disease in the tropical regions where the sickle-cell gene first emerged. Dr. Moalem discusses this example at length, as well as a similar genetic disorder called favism, an enzyme deficiency which produces severe anemia if its carrier consumes fava beans. Favism, like the sickle-cell gene, has become extremely common in some populations because it protects against malaria. Interestingly, according to the book, both genes work for the same reason: they make red blood cells more fragile and more stressed, turning them into a hostile environment for the malaria parasite.
Dr. Moalem’s other chief example is hemochromatosis, a genetic disorder that results in toxic amounts of iron accumulating in the body over time. Fortunately there is an effective treatment – old-fashioned bloodletting, which purges the excess iron from the bloodstream. Like favism, hemochromatosis is extremely common in some ethnic groups, and this leads naturally to the question of why. A uniformly harmful disorder would have been culled by natural selection, so by evolutionary thinking, its persistence must have conferred some survival advantage. And as the book argues, there is one. Iron is an essential nutrient not just for us, but for many species of infectious bacteria. When the body is under attack, part of its immune response is to deploy natural chelating proteins that bind to iron in the blood and take it out of circulation. As it turns out, hemochromatosis makes iron more concentrated in some organs, but makes it less concentrated in the disease-fighting white blood cells, making them more effective against deadly pathogens like those that cause tuberculosis and bubonic plague.
All of these are testable and relatively uncontroversial examples, but some of Dr. Moalem’s other arguments I find less convincing. For example, he argues that diabetes may have originated as an adaptive response to an ice age called the Younger Dryas that began suddenly around 13,000 years ago. As evidence, he discusses the remarkable example of the North American wood frog, a tiny animal that survives winter by literally freezing solid, then thawing out and resuming its life no worse for wear when spring comes. The frog accomplishes this by dramatically increasing the sugar concentration in its blood, which acts like a natural antifreeze to prevent destructive ice crystals from forming and rupturing its cell membranes and capillaries. The book’s argument is that diabetes may have originated to play a similar role in humans, offering a partial defense against frostbite in the cold.
This is a clever and intriguing argument, but I am not wholly convinced by it. For one thing, domestic cats and dogs can also get diabetes. Are we to imagine that it evolved in them for similar reasons? And if this thesis is correct, should we not expect to find dramatically higher rates of diabetes among the Inuit and other groups of people who habitually live at arctic latitudes? No such evidence is presented in the book, although if a study were done that found this to be true, it would certainly be powerful evidence in favor of Dr. Moalem’s argument. In the meantime, I remain skeptical.
With all that said, I have to register one fairly major objection to this book. In the final chapter, which is on aging and human birth, Dr. Moalem gives an unqualified endorsement to the “aquatic ape” hypothesis of human origins promulgated by Elaine Morgan. This hypothesis is a notorious piece of pseudoscience, and its supporters repeatedly make glaring errors of fact when arguing in its favor (see the previous link). As far as I am aware, the AAH is dismissed by virtually all qualified evolutionary anthropologists, and rightly so.
I myself can think of one major argument against this hypothesis. Morgan and others promote human hairlessness, subcutaneous fat, downward-pointing nostrils, and other traits as evidence that our species’ ancestors spent a substantial amount of time in an aquatic environment. Yet for all this, human beings lack a particular trait that would be far better evidence of aquatic origin than any of these, and one that we would certainly expect to be widespread if our ancestors evolved in the water: webbed hands. Doubtless, this would greatly improve humans’ swimming ability, which by all accounts is pitiful compared to genuine water-dwelling mammals. It would not be a complex mutation – all it would take is a little less apoptosis during fetal development. Why is this condition not far more common if the AAH is correct? It should be a normal human trait, not the result of rare birth defects.
I do not think Dr. Moalem is ignorant or a bad scientist. Instead, I think this is an example of an all-too-common phenomenon: the scientist who ventures outside their field of expertise and ends up making mistakes that an expert would have been able to point out. However, when he sticks to molecular biology and genetics, his specialty, his arguments are far more cogent and persuasive.