Evolution is the process of a species changing over time to better suit its environment. The mechanism of evolution was referred to as “survival of the fittest” by Alfred Russell Wallace, the codiscoverer of evolution. He thought that the term “natural selection,” coined by Charles Darwin, incorrectly implied a directed force behind the selection—i.e., an intelligent design. In a sense, what is most intelligent about the process of evolution is its utter simplicity: the ability to improve a species incrementally over thousands of generations, all through differences in individual rates of reproduction, aided by the raw material of random mutations.
Evolution gradually eliminates drivers who weave around on the freeway while yakking on a cellphone or typing on a laptop, or the more spectacularly foolish acts that earn Darwin Awards, like the men who tried to see who could hang the longest off a busy freeway overpass.10
There are many biological questions answered by evolution. For instance, humans apparently began wearing clothes seventy thousand years ago, according to the silent testimony of the lice that inhabit us. The human head louse lives on the scalp, while the body louse lives in clothing. The two lice genetically diverged when we began wearing fabric clothing, creating a new habitat. Researchers are now trying to date when humans lost their body hair, by analyzing the genes of pubic lice.
Chart by Nigel Holmes
Yet despite the evidence, creationists continue to use squirrelly logic (squirrelly: cunningly unforthcoming or reticent) to claim that there is no such thing as evolution. So let’s use our furry little friends, the squirrels, to illustrate the principles of natural selection.
In order for “survival of the fittest” to cause a species to evolve there are four requirements. 1) The species must show variation, and 2) that variation must be inheritable. 3) Not all members of the population survive to reproduce, but 4) the inherited characteristics of some members make them more likely to do so.
Wild adult squirrels can live about four years, and they have two litters of three pups every summer. Given these numbers, a single pair of squirrels could multiply to sixty-four quadrillion in thirty-three years if they all survived. That’s more than enough squirrels to blanket the entire surface of the planet! Obviously, most squirrels do not reproduce so prolifically.
If you spend time watching squirrels, you will see that some are fatter than others, some hide better, and some are more aggressive about obtaining food. Because not all squirrels survive to reproduce, there is a selective pressure that favors inherited traits that play a role in survival. The parents of each new generation are the most successful squirrels from the past summer. Thus, successful traits become more prevalent over time, and less successful traits eventually disappear.
Like squirrels, not all humans survive to reproduce. Case in point is the human who dies clutching a Darwin Award. Although we regret his passing, we claim (tongue in cheek) that he has done the rest of us a favor, by sacrificing himself, thereby ensuring that our children don’t have to breed with his children in the next generation.
ORIGIN OF THE NOVEL SPECIES NOODLEOUS DOUBLEOUS: EVIDENCE FOR INTELLIGENT DESIGN
Thomas D. Schneider, Ph.D.
Abstract
Penne rigate spontaneously inserts into Rigatoni (order pasta) under liquid to gas transition conditions of H2O to create the previously unobserved species Noodleous doubleous. The estimated probability of this spontaneous generation event is too low to be explained by thermodynamics, and therefore apparently represents Intelligent Design.
Introduction
Intelligent Design advocates* claim that patterns observed in nature with a sufficiently low probability of occurence provide direct evidence for intelligent design, i.e., God. Here I report evidence for the spontaneous formation of a new life form in a prebiotic pasta soup.
Materials and Methods
Two point five L of pre-filtered, activated carbon–filtered, and reverse-osmosis purified H2O was poured into a 24.0 cm (inner diameter) 4.7 L open metal nonstick-coated container to a final depth of 5 cm, and brought to 100 degrees C (liquid to gas transition). No NaCl was added. Forty pieces each of Penne rigate and Rigatoni were dropped into the boiling H2O. At five-minute intervals the mixture was stirred with a flat lignin paddle. At ~18 minutes the mixture was stirred a final time and then poured through a rigid plastic netting (square holes, sizes 3 mm x 4 mm and 4 mm x 4 mm) to capture the final products.
Figure 1: Sample of pasta captured from its native environment.
Figure 2: Final population.
Results
Figure 1 shows a randomly collected sample from the native environment in which several Penne rigate are inserted into Rigatoni. The sample pasta are suspended on the flat lignin paddle. Three Rigatoni (60 percent) contain Penne rigate inserts. Note that a portion of the environment can be observed on the right side of the image as a white froth containing gas-enclosed sphericals. It is impossible to observe the pasta through this froth without disturbing the environment. There is some evidence for ordered patterning of the environment in which the pasta are oriented vertically, but this was destroyed by stirring. Note that the H2O depth is substantially the same as the length of the two species of pasta.
Figure 3: Components of Noodleous doubleous. From left to right: dry P. rigate; dry Rigatoni; P. rigate sampled at eighteen minutes; example Rigatoni sampled at eighteen minutes; example P. rigate inserted into Rigatoni to create N. doubleous sampled at eighteen minutes.
Figure 2 shows the final population, in which 4 N. doubleous are visible. Conditions were no longer authentic al dente at the end of the experiment, and the violence of the trawling capture probably disturbed the neophytes. This could account for the reduced number of observed N. doubleous compared to the rapid sampling shown in Figure 1.
Figure 4: Dissection of Noodleous doubleous.
As shown in Figure 3, boiled P. rigate (length ~5.0 cm, outer diameter 1.0 cm) can just barely fit inside boiled Rigatoni (length ~5.3 cm, inner diameter 1.3 cm) with a clearance of perhaps 0.15 cm. Under the turbulent thermal conditions, sliding one pasta tube into the other should be strongly disfavored.
Figure 5: N. doubleous observed in heat-source-detached environment. Note three bubble plumes emerging from the dorsal end of Rigatoni tubes.
To examine the internal organs, an N. doubleous was dissected (Figure 4). We note that the two subspecies fit together closely.
The tissue of P. rigate is notably lighter than that of Rigatoni. Also evident was the smooth interior wall of Rigatoni.
To confirm the results, the experiment was repeated. In an attempt to observe native conditions, the environment was gently removed from the heat source without stirring. Although this allowed cooling, it is likely that the configuration of the pasta is similar to its configuration in the native frothy environment. Figure 5 documents two related phenomena. First, Rigatoni are frequently oriented vertically while many P. rigate are frequently oriented horizontally or at forty-five degrees to the vertical. Second, bubble plumes emerge from the dorsal end of Rigatoni tubes.
A calculation was performed to determine the probability of the observed insertion events (Table 1).
* * *
Table 1: IDIOTS** calculation
Rigatoni length (cm)
5.3
Rigatoni outer diameter (cm, from Figure 4)
1.7
Rigatoni cylinder surface
(length × outer diameter × π), cm2
28.3
Rigatoni cylinder ends
((outer diameter/2)2 × π × 2), cm2
4.5
Rigatoni total surface (side + ends), cm2
32.8
Inner diameter of Rigatoni, cm
1.3
The tip of P. rigate is pointy, with a diameter of 0.3 cm (Figure 3), reducing its effective size for slipping into Rigatoni. The target area the tip can enter:
(2 × π × ((inner diameter—tip)/2)2), cm2
1.571
Probabil
ity of one insertion during a random encounter is the target area divided by the Rigatoni total surface
4.78 × 10-02
Fraction of observed insertions (Figure 1)
0.6
Number of available Rigatoni
40
Estimated total number of insertions (40 × 0.6)
24
Probability of all these insertions by random encounter
2.05 × 10-32
** This calculation was performed according to standard Intelligent Design (IDiotic) methods. It was performed using the calc program with an input file “idiotic.calc.”
* * *
Discussion
This paper reports an observation of spontanoodlus generation in which Penne rigate inserts within Rigatoni to create a new species dubbed Noodleous doubleous.
The Vertical Flow Hypothesis proposes that Rigatoni become vertically oriented in the convective flow of phase transitioning liquid H2O, thereby increasing the heat dissipation rate.
This proposal is supported by the observation of bubble plumes on the dorsal side of Rigatoni (Figure 5). It is feasible that horizontally oriented P. rigate situated close to the bottom of the environment are drawn upward into the ventral side of Rigatoni. The P. rigate are not ejected from the Rigatoni because the dorsal end of the Rigatoni is close to the liquid surface and the process does not have sufficient energy to lift the P. rigate into the environmental froth. The P. rigate would therefore be caught inside the Rigatoni.
However, the probability of insertion events as proposed by the Vertical Flow Hypothesis is calculated to be extremely low (Table 1).
Conclusion
We conclude that the process was guided by some form of external intelligence. The experimenter did not perform this scalding task.
The high-temperature liquid was undergoing a rapid phase transition and liquid dihydrogen monoxide is extremely dangerous. Microscopic and macroscopic life forms were not observed in these extreme sterilizing conditions. Only an invisible macroscopic life form could have guided the rapid generation of the Noodleous doubleous.
We therefore conclude that this supernatural insertion process was done by the Hand of God.
A second viable hypothesis is that a divine Noodly Appendage of the Flying Spaghetti Monster was responsible for the effect. These results are therefore strong empirical support for Flying Spaghetti Monsterism.
Although it is considered unethical to destroy incipient life-forms, thereby causing them to go extinct, the experimenter was hungry, so he ate them anyway.
References, complete experimental conditions, further reading:
www.DarwinAwards.com/book/noodles.html
Church of the Flying Spaghetti Monster:
www.DarwinAwards.html/book/spaghetti.html
Essay on Intelligent Design by Jason Stevens:
www.DarwinAwards.com/book/jason.html
CLEANING THE GENE POOL
The Darwin Awards that follow show that Nature is still improving on the human design. But they also illustrate the creativity that distinguishes us from less adaptable species. The same innovative spirit that causes the downfall of the Darwin Award winner is also responsible for the social and scientific advances that make the human race great.
CHAPTER 1
Vehicles
Motorcycles, trucks, trains, cars, snowmobiles, mopeds, a wheelchair, and one mountain bike—wheels spark a powerful urge to test mechanical limits. But to begin, an essay on human evolution….
DISCUSSION: AIDS, BUBONIC PLAGUE, AND HUMAN EVOLUTION
Stephen Darksyde, Science Writer
Science 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 biology, 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 Darwin Awards 4: Intelligent Design Page 3
