Survival of the Sickest

by

Sharon Moalem

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Survival of the Sickest: Chapter 4 Summary & Analysis

Summary
Analysis
In ancient Greece, a variety of sources warned against eating fava beans, from Greek scholar Pythagoras to a cult called the Orphics (who believed the beans contained the souls of the dead). Moalem writes that these superstitions were not without merit. Favism is an inherited enzyme deficiency carried by 400 million people—the most common enzyme deficiency in the world. In extreme cases, people who have favism and eat fava beans experience “rapid, severe anemia that can often lead to death.”
The introduction to this chapter is reminiscent of Moalem’s discussion of bloodletting. While it is easy to dismiss these practices and beliefs as folklore of an ancient and less informed time, Moalem illustrates how they existed for a reason. Understanding the past, and how medicine or common knowledge has evolved over time, can provide evidence for some conditions in the present, as is the case with favism.
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Scientists first recognized some truth behind the aversion to fava beans during the Korean War. American soldiers were prescribed drugs to combat malaria, including one called primaquine. About 10 percent of African American soldiers developed anemia while taking primaquine, and other soldiers (mostly of Mediterranean descent) experienced an even more severe version called hemolytic anemia.
Again, in noting that most of the soldiers who developed anemia were of African American and Mediterranean descent, Moalem foreshadows his eventual reveal of the common factors that lead to favism and anemia. Just as diabetes was beneficial for people in ice age conditions of Northern Europe, it’s likely that there’s an underlying adaptation behind why these particular groups develop anemia from primaquine.
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Three years later, scientists discovered the cause of these side effects. The soldiers who reacted to the drug lacked an enzyme called G6PD, which clears out elements that are harmful to the cell. These elements include free radicals, which are molecules with unpaired electrons that can disrupt cellular chemistry. Primaquine is thought to stop the spread of malaria by preventing malaria-causing parasites from invading the body’s red blood cells. But with a lack of G6PD to maintain the cell’s defense systems, the cells become even more vulnerable. Hemolytic anemia can then lead to kidney failure, heart failure, and death.
Again, Moalem sets up the argument for why a disease like favism would be harmful, explaining some of the biology behind favism, anemia, and malaria. He illustrates why people have such a bad reaction to anti-malarial drugs, hinting at the idea that people who have favism don’t need to take primaquine because they already have a certain degree of defense against malaria due to their red blood cell vulnerability. This drug only makes that condition deadlier, without the added benefits.
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This lack of G6PD is known as favism, and it is named that way because when people who have favism eat fava beans, they undergo a similar reaction to the one that occurs after taking primaquine because of the free radicals in fava beans. The irony of favism is that the people who have favism are more likely to live in places where fava beans are cultivated: North Africa, Southern Europe, and around the Middle East (the countries that line the Mediterranean). Moalem again questions why humans would have evolved a mutation that causes problems specifically when eating a staple of their local diet.
In this case study, it is clear that like the other diseases, Moalem will ultimately prove how favism has an added benefit despite its potential harm. But there is an additional mystery that Moalem will also take on: favism’s relationship with people or places that create fava beans. This enables Moalem to transition to his discussion on how plants, animals, and humans can impact one another’s evolutions. Plants, he shows, have evolutionary purposes behind both their beneficial and toxic properties.
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Moalem then shifts to the broader connection between evolution in the animal kingdom and evolution in the plant kingdom. He notes that plants that produce edible fruit evolve that way for their own benefit: animals learn to pick the fruit, eat it, and deposit the seeds somewhere else so that the plants spread and reproduce.
This is Moalem’s first example of the symbiotic relationship between plants and the animals that eat them: animals who learn what parts of the plants are good to eat are more likely to survive, and the plants who develop fruit are able to move to other places and increase their species numbers.
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Plants have also evolved defense mechanisms so that the fruit is the only thing the animals eat. These mechanisms include thorns, but also chemicals and toxins that they have developed. Clover, sweet potato, and soy all belong to a group of plants that contain chemicals called phytoestrogens. These chemicals mimic the effects of sex hormones like estrogen, and the compounds diminish animals’ ability to reproduce. This ultimately proved useful to humans, however, as chemist Carl Djerassi based his development of the birth control pill on these hormones—specifically phytoestrogens produced by the Mexican yam.
Moalem’s next example illustrates how evolutionary adaptations can work in a kind of feedback loop: because plants develop fruit, animals eat the fruit and also try to eat other parts of the plant. In turn, then, plants must evolve mechanisms to prevent animals from eating the parts that are essential to them. This example also illustrates how evolutionary research can have broader scientific implications, as discovering how phytoestrogens protect plants from animals enabled chemists to develop the birth control pill. 
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Quotes
Plants also produce poisons to prevent predators from eating them. For instance, the cassava plant contains a precursor to cyanide, while the Indian vetch contains a neurotoxin that can cause paralysis. Plant toxins can also have milder effects, like interfering with digestions or burning lips. Raw habanero peppers have a chemical called capsaicin, which causes burning sensations in mammals but not in birds. This is because mammals’ digestive systems destroy the peppers’ seeds, while birds’ digestive systems do not.
Moalem illustrates how the development of capsaicin is designed to be the most helpful in evolutionary terms, guarding against only the predators whose digestive systems are harmful to the pepper’s seeds. Peppers’ adaptation developed in a way to prevent mammals from eating the peppers, but not to prevent birds from eating them so that they continue to deposit the seeds in other places.
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Humans will frequently still eat plants with toxins—between 5,000 and 10,000 every year—because we have also evolved mechanisms to manage those toxins. Tasting bitterness is one mechanism, as this ability allows us to detect toxins in plants and avoid eating them. However, not all compounds that are linked to bitterness are toxic—likely because most of the plants’ chemical weapons are aimed at insects, bacteria, fungi, and herbivores.
Moalem illustrates how plant adaptation has even affected the evolution of humans, as we have evolved to detect and manage the toxins that plants produce as a part of their defense mechanisms. Again, this emphasizes the interconnectivity of all species and how each one can spur another’s evolution.
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In the past, humans have tried to increase plants’ natural defenses in order to protect them from other predators like insects—sometimes with results that backfire. A potato was bred with more solanine (its natural poison), and it became so poisonous it was inedible. Celery defends itself with a toxin called psoralen, which causes sensitivity to sunlight in humans. It produces more psoralen when it feels under attack. For farmers who use pesticides, fewer insects attack the celery and it produces less psoralen. But organic farmers don’t use these pesticides, and ironically, refraining from external poison actually results in more internal poison in the celery plant.
In these examples, Moalem illustrates some of the dangers in trying to manipulate genes of other organisms to our benefit, because those manipulations may have unintended consequences. In this way, humans can inadvertently influence the expression of evolutionary mechanisms in an organism like celery that may not have manifested otherwise, once again showing the intimate connection between different species.
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Moalem returns to the connection between fava beans and favism. People who have favism and lack the G6PD enzyme cannot mop up free radicals, which results in anemia in more than 400 million people around the Mediterranean. However, this gives people an advantage over another common disease around Africa and the Mediterranean: malaria.
Here, as Moalem returns to favism, he also returns to his central thesis: favism is likely common (particularly around the Mediterranean) because it continues to prevent malaria, a disease that is even more deadly. In this way, it is similar to hemochromatosis (which protected against the bubonic plague) and diabetes (which helped primitive humans survive extreme cold).
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Malaria infects almost 500 million people and kills more than 1 million people every year. Malaria causes joint pain, vomiting, and anemia. Ultimately, it can lead to coma and death, especially in children and pregnant women. It was initially thought that malaria was caused by unhealthy vapors emanating from still water (malaria is old Italian for “bad air”). This theory was incorrect, but it led to the development of air conditioning by Dr. John Gorrie, hoping to eliminate that “bad air.”
The development of air conditioning serves as another example of how interdisciplinary research can be extremely beneficial—and even how incorrect theories on diseases can ultimately be helpful in sparking other innovation. Even though the cause of malaria is not actually air, this belief led to an essential modern innovation in the air conditioning.
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In reality, malaria is caused by parasitic protozoa which are deposited in the human bloodstream through mosquitoes. The most dangerous protozoan is called Plasmodium falciparum. Scientist J.B.S. Haldane was one of the first people to understand that certain groups with anemia have better natural resistance to malaria. Today, many scientists believe that a G6PD deficiency (favism) provides even more resistance because the red blood cells are less hospitable to the protozoa, and because they are taken out of circulation more frequently, disrupting the parasite’s life cycle.
Moalem provides the scientific explanation for why favism, and the resulting anemia, are beneficial in combatting malaria. This provides people with favism with a greater evolutionary advantage and a better assurance of survival, which is why people with favism are able to reproduce and pass on this enzyme deficiency.  
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Moalem then explores why the same populations with favism might have cultivated fava beans: he explains that favism is only passed on the X chromosome, and so many women only have one copy of the G6PD mutation. When someone with a partial or mild G6PD deficiency, or without the deficiency at all, eats fava beans, it makes the red blood cells less hospitable. Only women with two copies of the gene, or men with one copy, might have an extreme reaction to fava beans.
With this research, Moalem illustrates why favism is particularly advantageous: it is just as effective when one copy of the gene is passed on as when two copies of the gene is passed on. Therefore, most people receive the benefits of the deficiency through eating fava beans but do not experience the harmful by-products of the disease.
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Humans have long been relying on herbal remedies, but the first antimalarial medicine came from George Cleghorn in the 19th century, who found a remedy in the bark of the cinchona tree. A century later, French chemists found the beneficial compound, quinine, and made a tonic from it to prevent malaria. However, over time, nearly every strain of malaria has become resistant to quinine. Fava beans, on the other hand, are still effective because they alter human body chemistry, not the protozoa’s chemistry.
Moalem previously illustrated how plants and animals can influence one other’s evolution. This holds true for humans and disease-causing pathogens as well, as even when humans try to develop vaccines or medicines to prevent disease, those pathogens can frequently evolve resistance to those efforts.
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Many plant toxins can be harmful but also come with benefits: phytoestrogens can stop the growth of prostate cancer cells and may ease the effects of menopause. Capsaicin stimulates the release of endorphins, increases your metabolic rate, and can also serve as a natural painkiller. Psoralen in celery can cause skin damage but can also help psoriasis. Even common medications liked aspirin or taxol (an anti-cancer drug) are derived from plants. It’s helpful, Moalem concludes, to recognize the benefit that plants can afford to us.
Again, Moalem emphasizes the evolutionary compromises in our relationship with plants. Like disease, even though plant toxins can be harmful, they can also be helpful. The key is learning more and understanding when it might be necessary to accept the potential harm in order to receive the benefits—the same principle by which the diseases Moalem references have come to be inherited in humans.
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