Life has been on earth for billions of years. During that time huge numbers of organisms have lived and died. Fierce struggles between different lineages over the ages are supposed by Darwinists to have led to biological “arms races”—tit-for-tat improvements of the capacity to wage biological warfare, analogous to the sophisticated twentieth-century arms race between humans in the United States and the Soviet Union. Maybe the results of those biological arms races were sophisticated living machinery, far beyond what we would ordinarily think of as the result of chance.
That’s the theory. But it has proven extremely difficult to test adequately. Modern laboratory studies of random mutation/natural selection have suffered from an inability to examine really large numbers of creatures. Typically, even with heroic efforts by the best investigators, only a relative handful of organisms can be studied, only for a comparatively short amount of time, and changes in a few chosen traits are followed. At the end of such studies, while some interesting results may be at hand, it’s usually impossible to generalize from them. Although scientists would love to undertake larger, more comprehensive studies, the scale of the problem is just too big. There aren’t nearly enough resources available to a laboratory to perform them.
So, in lieu of definitive laboratory tests, by default most biologists work within a Darwinian framework and simply assume what cannot be demonstrated. Unfortunately, that can lead to the understandable but nonetheless corrosive intellectual habit of forgetting the difference between what is assumed and what demonstrated. Differences between widely varying kinds of organisms are automatically chalked up to random mutation and natural selection by even the most perceptive scientists, and even the most elegant of biological features is reflexively credited to Darwin’s theory.
Breaking the theoretical logjam would require accurate evolutionary data at the genetic level on an enormous number of organisms that are under ceaseless pressure from natural selection. That data simply hasn’t been available in the past. Now it is.
LEAPS AND BOUNDS
Even just ten years ago any attempt to locate the edge of evolution with any precision would have been well-nigh impossible. Too little was known. But with the relentless march of science, especially in the past decade, the task has become feasible.
A major difficulty of evaluating an evolutionary theory like Darwin’s has been that, while we can easily observe large changes in animals and plants, the reasons for those changes are obscure. Darwin and other early scientists could examine, say, alterations of finch beaks, but they couldn’t tell what was causing the modifications. Closer to our own day, mid-twentieth-century scientists could determine that some bacteria evolved resistance to antibiotics, but they didn’t know exactly what gave them that power. Only in the past half century has science shown that visible changes are caused by mutations in invisible molecules, in DNA and proteins. The only way to get a realistic understanding of what random mutation and natural selection can actually do is to follow changes at the molecular level. It is critical to appreciate this: Properly evaluating Darwin’s theory absolutely requires evaluating random mutation and natural selection at the molecular level. Unfortunately, even today such an undertaking is intensely laborious. Yet there is no other way.
The good news is that, with much effort and insight, modern science has developed the tools to do so. A triumph of twentieth-century science has been its elucidation of one requirement of Darwin’s theory—the underlying basis of variation. We now know that variation in organisms depends on hidden changes in their DNA. (For a summary of DNA structure, see Appendix A.) What’s more, scientists have catalogued myriad ways in which DNA can change. Not only can single units (called nucleotides) of DNA accidentally change when the DNA is copied in a new generation, but whole chunks of the double helix can accidentally either be duplicated or be left out. Very rarely all of the DNA in a cell is copied twice, yielding offspring with double the DNA of its parents. Other times active DNA elements resembling viruses can insert copies of themselves at new positions in the genome, sometimes dragging other bits of DNA with them. Opportunities for nature to alter an organism’s DNA are virtually boundless.
Not only has the hard work of many scientists shown the underlying basis of variation, the rate of mutation has been worked out fairly well, too. As a rule, the copying of DNA is extremely faithful. On average, a mistake is made only once for every hundred million or so nucleotides of DNA copied in a generation. But there are exceptions. In some viruses such as HIV the mutation rate is speeded up enormously.
Another critical advance in our ability to properly test Darwinism has come from DNA sequencing. In the past few decades the amount of DNA sequenced has been growing exponentially, and the number of organisms studied by sequencing has been expanded. In the mid-1990s the first complete sequence of an organism’s genome—a tiny bacterium named Hemophilus influenzae—was published. Now the sequences of hundreds of genomes are known. Not only whole genome sequencing, but the easy ability to sequence at least key pieces of an organism’s DNA gives scientists the ability to nail down the molecular changes that underlie genetic diseases, or that cause resistance to antibiotics.
Yet all that scientific progress would still not be enough to draw reasonably firm conclusions about the abilities of Darwinian evolution if sufficient numbers of organisms couldn’t be studied. The more organisms there are, the more opportunities random mutation has to stumble across a beneficial change and pass it on to natural selection, the firmer our conclusions about what Darwinism can do become. Studies of animals like finches can at best follow hundreds at a time. In the laboratory thousands of fruit flies might be examined. That’s better, but still far from enough. With thousands or even millions of organisms, a mutation comes along relatively rarely, and few of the mutations that do come along are helpful.
The natural world of course teems with organisms. There can be billions of a mammalian species on the planet at a time, such as humans or rats. In the seas there are huge numbers of fish. And these represent just the larger forms of life. There are also untold numbers of microscopic entities such as bacteria and viruses. While laboratories can’t grow enough creatures to get a reasonable handle on the abilities of Darwinian evolution, nature has no such problems.
Evolution from a common ancestor, via changes in DNA, is very well supported. It may or may not be random. Thanks to evolution, scientists who sequence human DNA and find mutations that are helpful—against, say, our natural enemies—are not just studying the DNA of one person. They are actually observing the results of a struggle that’s gone on for millennia and involved millions and millions of people. An ancestor of the modern human first sustained the helpful mutation, and her descendants outcompeted the descendants of many other humans. So the modern situation reflects an evolutionary history involving many people. When scientists sequence a genome, they are unfurling rich evidence of evolution—Darwinian or otherwise—unavailable by any other method of inquiry.
DARWINISM’S SMOKING GUN
Thanks to its enormous population size, rate of reproduction, and our knowledge of the genetics, the single best test case of Darwin’s theory is the history of malaria. Much of this book will center on this disease. Many parasitic diseases afflict humanity, but historically the greatest bane has been malaria, and it is among the most thoroughly studied. For ten thousand years the mosquito-borne parasite has wreaked illness and death over vast expanses of the globe. Until a century ago humanity was ignorant of the cause of malarial fever, so no conscious defense was possible. The only way to lessen the intense, unyielding selective pressure from the parasite was through the power of random mutation. Hundreds of different mutations that confer a measure of resistance to malaria cropped up in the human genome and spread through our population by natural selection. These mutations have been touted by Darwinists as among the best, clearest examples of the abilities of Darwinian evolution.
And so they are. But, as we’ll see, now that the molec
ular changes underlying malaria resistance have been laid bare, they tell a much different tale than Darwinists expected—a tale that highlights the incoherent flailing involved in a blind search. Malaria offers some of the best examples of Darwinian evolution, but that evidence points both to what it can, and more important what it cannot, do. Similarly, changes in the human genome, in response to malaria, also point to the radical limits on the efficacy of random mutation.
Because it has been studied so extensively, and because of the astronomical number of organisms involved, the evolutionary struggle between humans and our ancient nemesis malaria is the best, most reliable basis we have for forming judgments about the power of random mutation and natural selection. Few other sources of information even come close. And as we’ll see, the few that do tell similar tales.
(Caveat lector: Unfortunately, in order to fully understand and appreciate the difficulties facing random mutation, and how humanity’s battle with malaria illustrates them, we have to grit our teeth and immerse ourselves in details of the battle at the molecular level. I make every effort to keep technical details to a minimum, and some of them are confined to the appendices. But there is no way around the fact that this subject requires technical details.)
Although the number of malarial cells is vast, it’s much less than the number of organisms that have existed on earth. Nonetheless, as I will explain, straightforward extrapolations from malaria data allow us to set tentative, reasonable limits on what to expect from random mutation, even for all of life on earth in the past several billion years. Not only that, but studies of the bacterium E. coli and HIV, the virus that causes AIDS, offer clear confirmation of the lessons to be drawn from malaria. HIV, in particular, is something of a Rosetta stone for studying random mutation, because such viruses mutate at extraordinary rates, ten-thousand times faster than the mutation rate of cells. Viruses contain much less genetic material, but it mutates so rapidly, and there are so many copies of it, that HIV alone, in just the past fifty years, has undergone more of at least some kinds of mutations than all cells have experienced since the beginning of the world.
Most of this book will focus on the operations of cells and molecules, but in the last two chapters I go further. In recent years, as science has progressed at an amazing clip, some molecular details underlying the development of different classes of animals have come to light. I make some inferences about the limits of the use of random mutation to explain features of animal life. In the final chapter I show that the conclusions reached in this book about random processes in biology mesh well with recent results from other scientific disciplines such as physics and cosmology. Together they illuminate the role of chance in nature as a whole.
GLIMMERS OF THE EDGE
One difficulty of writing a book questioning the sufficiency of Darwin’s theory is that some people mistakenly conclude you’re rejecting it in toto. It is time to get beyond either or thinking. Random mutation is a completely adequate explanation for some features of life, but not for others. This book looks for the line between the random and the nonrandom that defines the edge of evolution. Consider:
On the one hand, there’s malaria. An ancient scourge of humanity, in some regions of the world malaria kills half of all children before the age of five. In the middle part of the twentieth century miracle drugs were discovered that could cure the dreaded disease and hopes swelled that it could even be totally eradicated. But within a decade the malarial parasite evolved resistance to the drugs. New drugs were developed and thrown into the fight, but with only fleeting effect. Instead of humans eradicating malaria, there are worries that malaria could eradicate humans, at least in some parts of the world, as the number of deaths from the disease increased dramatically in recent years. The take-home lesson of malaria is: Evolution is relentless, brushing aside the best efforts of modern medicine.
On the other hand, there is sickle cell disease. Although in the United States sickle cell disease is an unmitigated disaster, in Africa it shows a silver lining. It takes two copies (one from each parent) of the mutated sickle gene to get the disease. People who have just one copy do not have the disease, but they do have resistance to malaria, and they often live when others die. The gene that carries the sickle mutation arose in a human population in Africa perhaps ten thousand years ago. The mutation itself is a single, simple genetic change—nothing at all complicated. Yet despite having a thousandfold more time to deal with the sickle mutation than with modern drugs, malaria has not found a way to counter it. While the evolutionary power of malaria stymies modern medicine, a tiny genetic change in its host organism foils malaria.
On the one hand, there’s HIV. The human toll from AIDS in modern times is comparable to that from the Black Death in the Middle Ages. Modern research has developed a number of drugs to combat AIDS, but after a brief time—months, sometimes just days—they invariably lose their effectiveness. The reason is Darwinian evolution. The genome of HIV, the virus that causes AIDS, is a minute scrap of RNA, roughly one-millionth the size of the human genome. Its tiny size and rapid replication rate, as well as the huge number of copies of the virus lurking in an infected person, all combine to make it an evolutionary powerhouse. Random changes during viral replication, combined with the selective pressure exerted by medicines, allow drug-resistant varieties of HIV to prosper in a quintessentially Darwinian process. Here, evolution trumps medicine.
On the other hand, there’s E. coli. A normal inhabitant of the human intestinal tract, E. coli has also been a favorite bacterium to study in the laboratory for over a century. Its genetics and biochemistry are better understood than that of any other organism. Over the past decade E. coli has been the subject of the most extensive laboratory evolution study ever conducted. Duplicating about seven times a day, the bug has been grown continuously in flasks for over thirty thousand generations. Thirty thousand generations is equivalent to about a million human-years. And what has evolution wrought?
Mostly devolution. Although some marginal details of some systems have changed, during that thirty thousand generations, the bacterium has repeatedly thrown away chunks of its genetic patrimony, including the ability to make some of the building blocks of RNA. Apparently, throwing away sophisticated but costly molecular machinery saves the bacterium energy. Nothing of remotely similar elegance has been built. The lesson of E. coli is that it’s easier for evolution to break things than make things.
On the one hand, there are the notothenioid fish in the Antarctic region, which can survive temperatures that should freeze their blood solid. Studies have shown that in the past ten million years tiny, incremental changes in the fishes’ DNA have given them the ability to make a strange new kind of antifreeze—an antifreeze that sticks to seed crystals of ice and stops them from growing. A triumph of natural selection.
On the other hand, there’s (again) malaria. The fierce malarial parasite—the same evolutionary dynamo that shrugs off humanity’s drugs—has an Achilles’ heel: It won’t develop in its mosquito host unless temperatures are at the very least balmy, so it’s restricted mainly to the tropics. If the parasite could develop at lower temperatures it could spread more widely. But despite tens of thousands of years and a huge population size, much larger than that of Antarctic fish, it has not done so. Why can fish evolve ways to live at subfreezing temperatures while malaria can’t manage to live even at merely cool temperatures?
Somewhere in the middle of such examples lies the edge of evolution.
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ARMS RACE OR TRENCH WARFARE?
Not for nothing has malaria been nicknamed the “million-murdering death.”1 Every year it kills that many people—mostly young children—and sickens hundreds of times more. Human and malarial genomes have battled one another for millennia. Over the years billions of humans and astronomical numbers of malaria parasites have been at each other’s throats. In their intense, enduring evolutionary struggle, any mutation that gave one an edge over the other has been favored b
y natural selection and has increased in number. Thanks to techniques such as DNA sequencing, many of these molecular evolutionary changes in both humans and malaria have been brought to light. Far better than Galapagos finches, pretty peppered moths, or other, more appealing examples that capture the public imagination, malaria offers our best case studies of Darwinian evolution in action.
Like some microscopic Dracula, the diabolical malaria parasite literally feeds on our blood. A single-celled organism carried by mosquitoes, it enters the bloodstream when they bite us. Once inside, malarial cells circulate until they reach the liver, stopping there for a time in order to multiply. When back in the bloodstream, a malarial cell grabs onto the surface of a human red blood cell, seals itself tightly to it, pulls itself inside, wraps itself within a protective coating, and then starts feeding on hemoglobin. An infected blood cell can get stuck in our veins and stop circulating. Meanwhile, the malaria inside reproduces until about twenty copies are made. The score of new malaria cells break out of the (now trashed) red blood cell, re-enter the bloodstream, attach to other red blood cells, and start the process all over. Multiplying exponentially, in the next round four hundred cells are made. In a few days a trillion new malaria parasites can be produced and consume a large fraction of a victim’s blood.
The Edge of Evolution Page 2