The Darwin Awards 4: Intelligent Design (6 page)

Stephen Darksyde, Science Writer

S
cience teachers are often asked by skeptical students, “Why aren’t people evolving now?” The answer, of course, is that evolution works on time scales far outside of normal human experience. To witness dramatic changes in form and function would require a lifespan encompassing thousands of generations. And evolution would operate much faster if humans lived in small, isolated populations, where a new gene can take hold and spread rapidly.

Evolution has been described as “goo to you” or “monkeys to men.” But viewed as genetics, evolution is simply a change in the frequency of
alleles
(gene variations) in a population over time, as a result of natural selection. Humans number more than six billion. It would take many generations for a
single
beneficial gene to become fixed into that mass of humanity, much less enough genes to turn us into a new species. But we can observe a subtle change in gene frequencies happening right now as a consequence of natural selection. It involves AIDS, a gene for the chemokine receptor, and a mutant called Delta 32. And while some of those biogenetic terms may sound intimidating, with a dab of historical context and some basic bi
ology, the story behind them is both comprehensible and fascinating!

Around the same time that HIV was found to be fatal despite aggressive treatment of AIDS complications, physicians noticed a mysterious twist. In a minority of patients the disease progressed at a markedly slower rate. These lucky few seemed resistant, though not immune. Stranger still, when accurate tests for HIV were developed, it was found that an even smaller group infected with HIV never developed any symptoms! The race was on to find out why HIV killed most—but not all. The answer would take researchers to a surprising place and time.

Six hundred years before the first AIDS patient stumbled into an emergency room, Europe was in the grip of another epidemic, the granddaddy of them all: the Black Death. Victims developed grotesque swellings in the armpits and groin, often so severe that their skin split open and body fluids seeped out by the pint. Blood congealed in the fingertips, feet, and lips, turning them black. Death followed quickly. Within weeks, once bustling city streets were littered with decaying bodies. What medical facilities existed broke down completely. Entire sections of London and Paris were deserted as terrified residents fled to the countryside, spreading the plague to every village as they went. It was
The Night of the Living Dead
—only it wasn’t a movie. This was real.

The suspected primary culprit of the pandemic is
Yersinia pestis
, a bacterium carried by fleas living on rats which permeated the large, filthy cities of the era.
Y. pestis
infection does result in pronounced swelling of the lymph nodes, but it doesn’t explain everything. The pattern of infection, the geographic distribution of specific symptoms, and modern research on
infectious disease all suggest there was more ravaging the people of Europe than a single disease.

The Black Death, also known as bubonic plague, affects the immune system. As with HIV victims, the plague patient is an easy target for opportunistic diseases: typhus, tuberculosis, smallpox, flu. What may have happened is that these diseases and others suddenly found their environment—human bodies—greatly weakened by the initial outbreak of bubonic plague initiated by
Y. pestis.
And like any organisms handed an opportunity to expand their domain, they radiated and evolved furiously. The result might have been a veritable stew of new superbugs able to overcome the resistance humans had developed to prior strains over thousands of generations.

Hundreds of millions died during the reign of the Black Death, and yet mysteriously, some survived infection, and others were immune. These lucky survivors were the beneficiaries of adaptations that had evolved in their genetic code.

So what does the Black Plague have to do with AIDS? Infectious pathogens gain entry to their victim’s cells’ by slipping through the cell membrane, a semipermeable outer wall. HIV bribes a molecular doorman called the “chemokine receptor” to get in. The blueprints for these receptors are, of course, found in our genes. In the lucky few patients who resist HIV, it was discovered that a gene involved in the construction of the chemokine receptor is defective. Constructing fewer receptors means fewer welcome mats for HIV.

This gene comes in a pair, one from each parent. If an individual has a single copy of the defective gene, there are fewer chemokine receptors on the cells, and HIV cannot infect them so easily. If both copies are defective, there are no receptors at all, and HIV is shut down cold by the body’s defenses.

This life-saving genetic mutation, Delta 32, is found in higher frequencies in people with English, Scandinavian, and Germanic ancestry: the same population that took the brunt of the great plague. And as it turns out, the defective gene that we suspect conferred resistance to the Black Death all those centuries ago is the same one that gives resistance to HIV today!

In popular culture today, most people think of evolution as a fish growing legs, or monkeys turning into humans. In reality, only small changes occur from one generation to the next. But over time, those small changes add up. Eventually, the differences are large enough that an entirely new species splits off from an older parent population. Over really long periods, that process can transform a fish into an amphibian, or a tree-dwelling primate into a modern human.

Because of medical care, long generational spans, and a population in the billions, modern humans are evolving slowly, if at all. But given a big enough differential in mortality for selection to act on, we can pick up the pace as an evolving species. And more than five hundred years ago, in the midst of an epidemic that knocked off 25 percent of everyone alive, that’s
precisely
what may have happened!

The stories in this chapter show that humans still have a long way to go in evolving to cope with the ubiquitous dangers of our transportation system. Vehicles can be hazardous to your longevity!

Michael, 27, was spending a pleasant afternoon cruising on his motorcycle, and witnesses who saw him speeding down Meridian Avenue were not surprised when state troopers reported that he had lost control near the Kapowsin highway. You see, he was steering with his feet. Michael was killed instantly after being thrown from his motorcycle, which had veered to the right and hit a guardrail.

Reference:
Tacoma News Tribune

Most rutting contests involve two male mammals, like the Rocky Mountain bighorn sheep,
Ovis dallis
, which ram each other at high speed in order to impress a female sheep and win the right to procreate. These mammals tend to have unusually thick skulls and extra fluid surrounding the brain to prevent damage from the competition. Humans tend not to have such thick skulls and other natural adaptations, and therefore do not generally rut.

Of course, man, the tool user, can find artificial means to overcome natural limitations. One well-known example of this behavior is the medieval jousting contest, in which participants wear armor and ride horses toward each other at high speed.

The most recent observation of human rutting behavior occurred when two Taiwanese university students donned protective helmets and revved their motor scooters in an effort to impress a comely female of their species. The two were in the same class, but were not friends. Other classmates reported that both men fancied the same female student.

After indulging in a few drinks during the Mid-Autumn Festival, the two encountered each other, and words were spoken. The gauntlet was thrown down. In lieu of horses, the two would ride their motor scooters at each other at high speed, and the one who didn’t turn away would win the exclusive right to pursue the female.

Obviously, both were very keen on her, because neither of them turned away. Their scooters collided head-on at fifty miles per hour. Both died instantly. The girl at the center of the rut refused to comment, other than to say that she “wasn’t interested in either of them.”

Reference: Major Taiwan media

When Peter and Jesse wanted to see what their new ride could do, like many young men, they got more than they bargained for. It was all fun and games until the vehicle stalled. In most cases this wouldn’t be a serious problem—but Peter and Jesse stalled at forty-one thousand feet.

You see, they weren’t pushing the old man’s car to the limit. They were flying a fifty-passenger jet, a Bombardier CRJ200. Fortunately, there were no passengers aboard to share the fatal consequences.

Jesse, thirty-one, was the captain of Pinnacle Airlines Flight 3701, and Peter, twenty-three, was the copilot. They were transporting an empty plane from Little Rock, Arkansas, to Minneapolis, where it was needed for a morning flight. They decided to see what that baby could do. Their fun began while ascending, as they pulled 1.8 Gs in a maneuver that activated an automatic stall avoidance system.

Then they decided to “forty-one it,” which meant taking the jet to forty-one thousand feet—eight miles—the maximum altitude the plane was designed to fly. The thrust of the engines pressed them into their seats with 2.3 times the force of gravity as they soared ever higher, laughing and cursing in a friendly manner, ignoring the overheating engines and the stick shaker that warned they were operating outside safe aerodynamic parameters.

At this point, air traffic control contacted the pilots to find
out what they were up to. A female controller’s voice crackled over the radio: “3701, are you an RJ200?”

“That’s affirmative.”

“I’ve never seen you guys up at forty-one there.”

The boys laughed. “Yeah, we’re actually a, there’s ah, we don’t have any passengers on board, so we decided to have a little fun and come on up here.”

Little did they know that their fun was doomed when they set the autopilot for the impressive climb. They had specified the
rate
of climb rather than the
speed
of the climb. The higher the plane soared, the slower it flew. The plane was in danger of stalling when it reached forty-one thousand feet as the autopilot vainly tried to maintain altitude by pointing the nose up.

“Dude, it’s losing it,” said one of the pilots.

“Yeah,” said the other.

Our two flying aces could have saved themselves at that point. An automatic override began to pitch the nose down to gain speed and prevent a stall. Regrettably, Jesse and Peter chose to overrule the override. Oops. The plane stalled.

“We don’t have any engines,” said one.

“You gotta be kidding me,” said the other.

Jesse and Peter still might have saved themselves. They were within gliding range of five suitable airports. Unfortunately, they did not reveal the full extent of their difficulties to the controller. They said that they had lost only one of the two engines. They glided for fourteen full minutes, losing altitude all the way. As they drifted closer and closer to the ground at high speed, still unable to get the engines restarted, they finally asked for assistance: “We need direct to any airport. We have a double engine failure.”

Unfortunately, it was too late. “We’re going to hit houses, dude,” one of pilots said, as they desperately tried to reach an airport in Jefferson City. They missed the houses and the runway, crashing two and a half miles from the airport. Both men died in the crash.

“It’s beyond belief that a professional air crew would act in that manner,” said a former manager of Pinnacle’s training program for the Bombardier CRJ200.

Reference:
New York Times,
NTSB, aero-news.com

Men seem to have an affinity for large trucks. What else can explain the actions of a thirty-four-year-old thief who decided to take possession of the engine of an old Bedford tip-truck?

The truck was parked outside a glass recycling company in Alexandria. It generally takes three men to lift an engine block of this size, but our enterprising pilferer decided that the best way to remove the engine was from below, rather than the conventional out-the-top-with-a-hoist technique.

He crawled under the cab and began to loosen the bolts.

Suddenly the engine block broke loose and landed on his face, killing him instantly. Police ascertained that he had at least one accomplice, judging by the pool of vomit found under a nearby bush.

An employee discovered his body early the next morning. The manager said that the truck was about to be scrapped. “If he had come and asked me for it, I would have given it to him.”

Reference:
Australian Police Journal,
Vol. 53, No. 2, June 1999

 

Readers comment that an engine block can’t drop without removal of the whole drive train and cutting out the motor mounts and bracing. Possibly it was the transmission or gearbox that fell on him, not the engine.