How Did Life Appear on Earth?
This page is part of my topics in biology pages. For comments or suggestions, email to the author.
|It has long been suggested (since
1859) that the existence of living beings on this planet
— you know, those wonderful creatures starring in the
documentaries of the Discovery channel, filling our
leisure time with awe and amazement — is not
due to some capricious decision made by a supreme
Designer, who, one day thought “Let’s make the Earth
give forth plants and animals.” Instead, it was
suggested that all species (including Homo sapiens,
members of which are the author of this page, and you, gentle reader) evolved
out of earlier ancestor species. Moreover — so that
theory goes — all living creatures share a common
ancestor, and their evolution is determined by purely
natural mechanisms, not supernatural ones. Although
scientists whose purpose is to study these issues (i.e.,
biologists) show a nearly unanimous agreement on the
correctness of the general principles of evolutionary
theory, some laypeople are reluctant to accept this idea.
“What? We, the crown of Creation, descended
from monkeys?!” It is an appalling thought, to many, to
think that we might not have been specially designed by
an all-caring, loving, supernatural, and intelligent
So laypeople often think that, even if species change throughout the millennia, such changes might have been “helped”, or “directed” toward a predetermined goal at the right moment by the Intelligent Designer. Others refuse to accept the very idea of change among species, in spite of the overwhelming evidence brought forth by biologists, paleontologists, and geologists. “Anyway,” say evolutionary disbelievers, “even if evolution does happen, and species do change through time, nobody can explain why life exists on Earth in the first place. Who placed it here? Who created the first living being? And who started off evolution, knitting it in the fabric of biological life, so that it can be discovered as a ‘theory’ in our times?” It is the purpose of this text to show that there are answers to these questions. It can be explained how life appeared on Earth. In a paradoxical manner, evolution contains within itself the explanation for its own existence. To understand it, one needs no special training or scientific knowledge, but mere common sense and rational thinking. If you decide to read on, you might be surprised to find out that the explanation will provide answers to other, seemingly unrelated questions: why all creatures — including the majority of humans — want to live? Why no animal ever chooses to die? And why, contrary to our will, we die eventually?
Have you ever entertained the thought that you might decide, for no reason at all, to drop yourself under the wheels of a passing car? This thought once crossed my mind but it wasn’t because of depression — psychologically, I am a very balanced person. It just popped out of nowhere one day among my thoughts, without warning, while I was walking along a busy street. At once I felt very uncomfortable having such a horrible thought in my mind, pondering its dire consequences for my immediate relatives, and the people I love. Although human beings are the only members of the animal kingdom who have the “privilege” to be able not only to think such thoughts, but also carry them out (under stressful psychological conditions), no other living being seems ever to consider this possibility: all creatures appear to be always striving to survive.(1) Why?
In what follows I will attempt to show first that life didn’t spring out of nowhere on Earth, as a whimsical decision of a Supreme Architect, but that it is a natural consequence of the fundamental laws of chemistry. Nor is evolution some special sort of “law” that was placed upon biological life for unknown reasons. Evolution is also a direct consequence of the laws of chemistry. That is, given the structure and properties of atoms and molecules, and certain suitable conditions, evolution is bound to happen, just as rain comes given suitable atmospheric conditions, without anyone “ordering” it to drop on earth. A consequence of this idea is that — assuming chemistry works the same way everywhere in the known universe — we should expect biological evolution to appear — or have appeared — elsewhere in alien worlds, given the right conditions. Notice that the claim is not that every alien evolving biological system — if any exists — has to be using the particular mechanism through which evolution was implemented on Earth, namely, our wonderful DNA molecules and the rest of our specific biological machinery. The implementation of evolution might differ in the details from place to place, but the fundamental evolutionary principles have to be the same. Along the way in our discussion I will provide an explanation for why species want to live and not die, and for why procreating, finding food, and avoiding predators seem to be such all-important, life-long, and life-consuming activities.
Let’s start with a thought experiment. Suppose we put a number of colored balls on a table, and shuffle them so that there is no particular pattern formed by the colors. Figure 1 shows such an arrangement.
Figure 1: A random arrangement of balls in motion
The balls keep moving randomly on the surface of the table, jostling and bumping against each other. Now, my plan is to have each of those balls represent a molecule — for example, they could be molecules of water, methane, ammonia, carbon dioxide, and so on — so I’ll drop the fancy term “colored ball”, and call them “molecules” from now on. Each color represents a specific type of molecule. For instance, the blue ones could be the water molecules; but we don’t care really which color stands for which type of molecule because we want to assume there are several types (colors) and a fair number of molecules of each type.
Imagine now that when our molecules bump against each other chemical reactions take place. Some times the blue ones join with the green ones and give a new color (a new type of molecule), for example, orange; then the orange ones may join with the yellows and break down in a specific way, giving two different types; and so on. In short, chemical reactions take place, causing the colors on our table to change continually, with no apparent plan, no purpose, no design or pattern. If you pay close attention to the molecules in figure 1 you'll see them gradually changing color, after each collision. Notice, however, that the reactions (color-changing) all comply with the laws of chemistry. For example, a methane molecule and two molecules of oxygen (say, one green and two reds) will always yield two water molecules and one carbon dioxide (say, two blues and one yellow). There is randomness in the collisions, but no randomness in the outcome of a chemical reaction.
So our table-world goes on like this for quite some time. Compound molecules tend to become more and more complex, especially since one of the elements, the carbon atoms, tend to cluster in “chains”, “rings”, and “branches” of arbitrary length, allowing other molecules to cling onto those structures. Colors come and go, appear and disappear, new colors emerge which hadn’t been seen before, but no particular color “dominates” the others, since each type of molecule has a random choice of possibilities: either joining with others, or breaking down in some way, thus yielding different colors on our table. The activity goes on for a long time, and complexity in molecular structure keeps increasing, until... one collection of molecular types makes an initially inconspicuous appearance.
This kind of molecule, which will be depicted in the figures that follow with hues of purple color (and a little mark on the center, you’ll see later why), has a property that none of the other molecules had before — at least not to such an explicit degree: when a molecule of this kind reacts with other molecules on the table, instead of breaking down in a haphazard way, it makes a copy of itself. The copy is not perfect. We’ll show differences in structure between the parent molecule and its copy as differences in purple hues. The point is, however, that parent and clone molecule look very much alike, and both continue existing and reacting after the cloning. There is nothing miraculous in having a molecule cloning itself.(2) A molecule can “achieve” this by first gathering various other simpler molecules from its vicinity, thus growing in size. The growth in size causes some of the bonds between its atoms to weaken, so when it reaches a certain critical size it splits, and two nearly identical copies of the original purple molecule are made. The two purple ones go on gathering scraps of molecular debris from their environment (not because they “want” it, but because this is dictated by their chemical structure), and continue growing in size, just like the original molecule did. When they have gathered enough material they split again, yielding four purple molecules where there had been only two before. This sequence of chemical reactions continues for awhile, resulting in eight, then sixteen, then thirty-two varieties of purple, and so on, with their numbers increasing like this, “geometrically”. Of course, not all of them manage to complete their scrap-gathering-and-split cycle, because they just don’t happen to bump against the right kind of scrap to add on to their bodies, or they actually break down when they meet with a few molecules that react by taking chunks out of the body of our poor purplies (which thus cannot continue their normal chemical cycle because their structure is altered). More important, several of the clones are not faithful enough replicas of their parents, and so are not capable of cloning themselves. A few of them, however, can have even better cloning abilities than their parents (just out of pure chance: a person can be taller than both of his or her parents). Such “better replicators” will tend to increase in numbers, precisely because they do a good replicating job, at the expense of “worse replicators”, the population of which will tend to wither away. It is those “good” replicator molecules that contribute to the increase of the purple population.
Not very long after the appearance of the first purple molecule, a dramatic change starts becoming evident on our table: where there was no pattern before and colors were changing randomly, now the purple molecules tend to persist as a color. A glance at our table suffices to notice this change (see figure 2).
Figure 2: Purple molecules prevail
But note that if you view this figure a long time after the page was loaded, some purple (replicator) molecules may have “mutated” and taken on different colors. However, all replicators are depicted with a little square at their center, contrary to other molecules which don’t have that mark. To start anew, reload the page.
What has happened? At the chemical level, nothing really changed: just as chemical reactions were happening before, chemical reactions continue to occur now. However, at a higher level of description, which we call biological, things started appearing that are worthy of new words for their description. For example, it looks like these purple molecules “want” to find scraps of smaller molecular debris (shouldn’t we call those “food”?) in order to grow and eventually split in two, replicating themselves and starting all over again. It’s not that they really “want food”, of course — they’re just molecules, after all, like every other type on the table: every molecule or atom, no matter how simple, might be seen as “wanting” to “eat food”. For instance, an ordinary atom of sodium may be seen as “wanting” an atom of chlorine, to make a molecule of salt. The same thing happens with the purple molecules: they “want” the molecular pieces which they can bind with (some of which, occasionally, cause them to break down). But by virtue of being the only ones that clone themselves, they appear as if they succeed in increasing their population. Hence, the population of purple molecules appears as if it wants to keep existing and growing, at the expense of other kinds of populations, which do not have such “desires” because their molecules simply change randomly from one type to another. Notice that now we can start talking about the whole population “wanting” to do something (to exist), while before we couldn’t ascribe such an attribute to populations of non-replicating molecules.
Thus, we started talking about populations of molecules “wanting” things, such as to keep existing, “to live”. The reader might feel the verb “want” is too heavily loaded with human-related values, and we are not justified in using it for collections of molecules. True, but is there a line we can draw among animals and say that some of them really “want” things, while others simply react? Does a dog “want” a walk? Who can resist describing it as volition when our poodle scratches on the front door at the time of her afternoon walk? Does a parrot “want” to detach the seeds from the bird-feeder? Does a shark “want” to attack? Does a spider “want” to spin its web? Does an amoeba “want” to engulf a scrap of food, invisible to our eyes? Where do we draw the line? Maybe the best option is not to draw any line at all, allowing such words have a wide range of meanings, from the simple, to the most complex. The advantage of doing so is that we don’t have to invent new words for the various shades, nor do we have to make arbitrary decisions about where to draw the lines. According to this approach therefore, yes, a particular population of molecules wants to survive, wants its members (molecules) to find food, and wants to do so at the expense of other populations.
Hence we come to a point where we can discern the underpinnings of our most fundamental biological functions. We want to eat and grow because our earlier ancestors (including the earliest forms of non-living chemical compounds) “wanted” to “eat” and grow. In an even more fundamental sense, eating is none other function than the mere binding of atoms and molecules. Whether it is hungry Joe devouring a Big Mac, or a molecule of glucose making covalent bonds with a hydrogen atom, the principle is the same. Except that Joe calls the satisfying of his needs “eating”, while the glucose simply “binds” with hydrogen.
It’s time we put these ideas together in a program, similar to figures 1 and 2, but which you can interact with. The program will start with a collection of molecules, all of which will be “plain vanilla” (non-replicators), as in figure 1. You can fill the space with such molecules by clicking on button , at the top-left of the program’s area. Then, when you click on , the molecules will be set in motion, starting to bump and react against each other, gradually changing colors (i.e., their nature). The possible colors available to our molecules are shown in the next figure:
Figure 3: Colors (types) available to molecules
“Hue = 200”, on the horizontal axis, means that the color is purple. “Sat = 236” (i.e., saturation) on the vertical axis means that the color is fairly rich in content (low saturation, close to 0, means the color is washed out, or grayish). Finally, “Lum = 150” (i.e., luminosity) on a separate axis on the right means the color is neither too bright (whitish), nor too dark (blackish).
In figure 3 we see all possible colors arranged in a square. A tiny portion of this square (very close to the top line and on the right, within the area of purple color) has been singled out with a little black rectangle, barely visible. Any molecule the type of which belongs to that area, will be a replicator. Initially, as we said, no molecule will be of that type, but as they react by bumping against each other and change colors, you can think of them as “moving” in the above colorful square (this is a conceptual motion, of course, as opposed to their real motion in space). Thus, by chance, a molecule while “moving” (changing type) in the above color space, might find itself within the tiny black rectangle, and thus acquire the property of replication. Once there, it may bump against “food” while wandering in space, and thus grow, split, and produce a copy of itself (another replicator), or it may not find enough “food”, bump against some “poisonous” molecule and break down, becoming potential “food” for others. Go on! Try the program.
Note: As soon as you press on Start, figures 1 and 2 will freeze, to free up computer resources and make motion in this program smoother. They will continue moving as soon as you pause this program.
You might have to wait for some time before the first replicator appears. When I try the program, I get the first replicator at any “epoch” (= one step in space for all molecules) between 100 and 1000, but it can happen really at any time, since the motion is random. You can see the epoch number on the status line (at the bottom), as well as the overall number of common and replicator molecules. Experiment by changing the parameters of the program (initial number of molecules and and their size, which determines the space size, accordingly), to see how the arrival of the first replicator varies in time. Note that although the first replicators will look like this , soon some of them will “mutate” (the copied version will be imperfect, hence slightly changed in type), and so various strains of colors will appear — all discernible as replicators through the tiny black rectangle at their center. A few of those strains will be better survivors than their parents (e.g., because they are a little more resistant to poisons and thus last longer before breaking down, or because they can consume food a little more efficiently, and so on). So, over time, you’ll see those strains, having a survival advantage, to dominate in our space before being surpassed by even better survivors, etc. Once again, all this will not happen because they “want” it, but because it is dictated by the statistics of their chemical nature. There is nothing in the code of this program that dictates replicators to live longer. All each replicator in this program has is a copying fidelity factor, an “endurance”, and something like “enough food in order to split” factor, all three of which are direct consequences of its type.(3)
How many can the replicator molecules become? Can they “eat up” all other molecules, thus turning everything into a replicator? If our space has borders, as most real spaces do, this is impossible. The reason is that the supply of “food pieces” (non-replicating molecules) is limited. Sooner or later the food pieces will start becoming sparse, and the replicator molecules will not be able to “eat” anything: they will start drifting aimlessly for some time, until they bump into some dangerous substance (some special “poisonous” molecule, replicator or not) and break apart, making a few chunks of “food” for other replicators with the pieces of their bodies. Eventually the numbers of the two categories (replicators and plain molecules) will come to a balance point. With the default values for the parameters in the program above, I observe a balance at around 780 replicators and 220 plain molecules.
We are ready now to answer the question posed by the title of this page. Why do we want to live?
Why does an animal, plant, bacterium, or any species at all, want to live? Could we find the answer by thinking about our populations of replicator molecules? Do they want to live?
Consider what would happen if any one of the replicating varieties had the tendency (by a hard luck due to a mutation in chemical structure) to break apart while growing before maturing to the size that is critical for splitting. Such a hapless individual would not produce descendants. Which means that the deleterious mutation that led to its formation would result in an individual incapable of self-replicating, and that would be the end of the story — and of the mutation. Only mutations(4) that allow the individual to split can be carried over to its descendants, and hence, get propagated to future generations. Therefore, the only individuals that manage to form viable populations are the ones that live to reproductive age. For our molecules, “living to reproductive age” means growing to the point of reaching a critical mass, and then splitting. So the “desire” to live, at least up to reproductive age, is a necessary built-in feature of all survivors. The only creatures that are not “interested” in living are the ordinary non-replicating chemical molecules.
Fine, but do animals live only to reproductive age? That is certainly not true: animals (and plants) don’t die immediately after giving birth — at least not the ones we are most familiar with. Furthermore, we know from personal experience that we humans do not give up the desire to live right after the birth of our children. How can the “desire” of the purple molecules to live to reproductive age ever be compared with our desire to live forever?
And yet it can, because the difference has to do with biological complexity. Along the path that connects us, monstrously complex mammals, with them, simple first invisible replicators (a path than extends for approximately four billion years to the best of our knowledge), some changes occurred. One of them was the “discovery” of sexual reproduction. Until around 2,100,000,000 years ago, all species were replicating just like our purple molecules: by splitting. Somewhere at that time, give or take a few dozen million years, a new mode of reproduction appeared: replicating by combining genetic information (that is, molecules) from one “male” and one “female” individual. Why? For the same reason all innovations appeared in our multi-billion-year evolutionary history: because it offered advantages in survival. We do not need to go into details here, explaining what those advantages are. Suffice it to say that what is involved is not the survival of individuals such as me and you, but of the genes (molecular chunks of information) that we carry and want to transmit to future generations. The story of gene replication and propagation is a very important one, and we’ll need to understand it in order to be able to appreciate the answers to questions such as the one posed in this text. For now, however, it’s sufficient to observe that humans (and many other species) do not produce clones of themselves by splitting in two like the original replicators, but make children by combining genes from a female and a male. Thus, we do not cease to exist immediately after giving birth, for various reasons. For one, we may give birth to more descendants later, and that means making more copies of our genes. For another, we need to take care of our children, making sure they’ll live well and produce their own offspring (thus furthering the lineage of our genes). And even long after reproductive age, our existence may prove useful to our offspring by taking care of our grandchildren, a practice which is common among social animals, such as humans, chimps, and gorillas. Hence, we don’t want to die, ever. Many other animals do not live much longer after giving birth. (Some, like the Alaskan salmon, die right there, on the spot, after reproduction.) But if any living being ever wanted to die before passing on its genes, neither itself, nor its descendants can be among us to witness their existence.
Let us keep thinking a bit on this point, because with what we observed so far we can see the answer not only to the question “Why do we want to live?”, but also to the one asking “Why do we die?”. Here is why we eventually die, in spite of all desire to live forever.
We noted that of all mutations that happen to molecules when they replicate themselves, those that are beneficial for their survival are bound to be propagated to their descendants (because they result in better survivors), while those that are detrimental and show their bad character before the molecules clone themselves are bound to be eliminated (because molecules of such nature will not replicate, or will replicate erroneously, resulting in non-viable populations). But what about those mutations that are detrimental but do not show their effects until some time after the reproductive age of the molecule? There is nothing in what we’ve seen so far that labels such mutations as “bad”: they may result in “killing” the molecule at a later stage, but it first manages to produce descendants, all of which will carry such “killer mutations” (being copies of their parent), which will not affect their ability for procreation! And so, “killer mutations of old age” will keep accumulating in all strains of replicators.
Did the word “cancer” pop up in your mind while reading the above lines? Tumors are a very complex phenomenon, not yet fully understood, but their appearance complies to the same basic outline, as expressed in the previous paragraph.
I once had a cousin, one year younger than me, who died of intestinal cancer at the age of nine. A couple of years later, another cousin of mine, and best friend of my childhood, died of an aneurysm in his brain at the age of thirteen. Those losses were devastating to me and my relatives, and I couldn’t swallow in my child’s mind the idea of “What kind of cruel God this is, who lets innocent children die!” Little did I know that God — whether existing or not — does not have to be part of the picture, nor does any god have to be implicated to the luck of individuals. It’s all statistics. We all have those “bad genes” in our bodies. Their effects are usually expressed gradually, and cumulatively as we age, both in mild forms (freckles on the dried, wrinkled skin, accumulation of salts in the joints, blocking of the arteries, etc.), and in more severe ones (tumors, Parkinson’s and Alzheimer’s diseases, heart attacks, and many others). Generally, however — and fortunately! — children do not develop tumors nor degenerating diseases. In the very unfortunate case that they do (because statistically even the worst kind of luck is bound to strike a small enough number of individuals), they do not live to reproductive age and do not pass their unfortunate luck to any descendants. The rest of us carry on our (accumulated through billions of years) bad genes, which express themselves seemingly “conveniently” long after we give birth to our children, and after we (“conveniently”, again) are given some time to take care of them, and make sure they live well and prosper.
The reader may now object with this logical argument: why didn’t evolution “take care” of bad mutations? Wouldn’t it be beneficial to individuals to go on living forever, and thus keep producing descendants on and on? Wouldn’t that strategy result in even more viable, impossible to eliminate populations? Why didn’t such bad-gene-free populations ever appear?
The result of living on forever would be that the number of individuals of a given species would keep on increasing. But is this possible? After the number of individuals reaches a maximum value, food in the environment is repleted, and members of the species start starving and die. (See how this happens to the various colored types in our program, above.) So the number of individuals gets checked by the availability of resources in the environment. There is no built-in evolutionary principle that says “We have to have as many individuals of our species as possible!” All that there is, is that species that are better equipped prevail, purely statistically, over their competitors (and that’s a mathematical certainty, not a law of nature, which we observe but don’t know why it’s there). That’s all. Thus, what appears to us logically as “a good thing to have” (i.e., living forever), is not something derivable from the structure of the material we are made of. Living forever would be something we would expect from a Designer to grant us, if such a creature had actually designed us and cared for our well-being, for our fear of death, the sorrow we feel for our deceased loved ones, and so on.(5) But instead of being made by a Designer, we sprang out of the un-caring, un-planning ahead forces of nature. Evolution doesn’t have any provision to look ahead and plan for the future, nor sense our desires and satisfy them. It’s a blind natural mechanism that makes use only of what works here and now. In all fairness, evolution did make us, large mammals, to be able to live long after we give birth to our children, and take care of them. Most other living beings don’t have this luxury. But those “bad genes”, the little time-bombs waiting to explode in time as we age, were there from the beginning, never completely eradicated by evolution because the current scheme of things works (as far as propagation of our genes to our offspring is concerned). So we die.
Note please that the theory of “bad genes that act as time-bombs” is only one of the theories that explain why we age and eventually die. There is at least one more, quite convincing one. As each cell in our bodies must at some point divide and produce two copies of itself, it does so inaccurately. That is, minor mutations are introduced in the DNA’s of each of the two copies. This is unavoidable, because although nature has mechanisms that ensure faithful copying, its mechanisms are not perfect. The copying of cells happens throughout our lives. So, copy after copy, as the years pass we end up with cells whose DNA is worse and worse as a copy of the original DNA, the one we inherited from our parents at the time of conception. It’s like getting a photocopy of a photocopy... and so on, for a very long time: each tiny speck introduced in one of the copies is carried over to all successors. Individually, the late copies of cells are not easy to identify as faulty. But when asked to work as an integrated whole (in body tissues and organs), their tiny faults become a problem in the way they cooperate with each other. Thus, an old muscle is made of cells that, being thousands of copies away from the original, do not cooperate in as perfect a way as they were “expected” by the original blueprint. Note that a heart, too, is a muscle, so it can fail at some point and lead to the death of the individual. But operational failures don’t need to be lethal to be noticed. Even the overall appearance and change of our bodies as we age can be understood in the light of this observation.
|I would like
now to go back to a point, which the reader may consider
as very crucial, because most of what we have seen so far
rests on it. The reader might object like this: “You
have attempted to explain how life appeared on Earth by
postulating the existence of a first replicator. But how
could the first replicator arise? Out of chance? That
would be like winning in a lottery where your chances are
one in a trillion, or who knows how much less. You have
pushed the appearance of life back from the first living
cell to the first replicator molecule. That doesn’t
explain where the first replicator came from.”
But wait! This objection accuses me wrongfully of things I never said. There was no first replicator. What this means is that replication is not a black-and-white, all-or-none property, that molecules are either capable of or not. There can be shades of gray in the ability of how good a molecule can replicate. On one side of this range stand molecules which, after reacting and breaking down, result in pieces that do not look at all like the original ones. Most inorganic molecules belong to this side of the “replicating range”, i.e., we clearly don’t call them replicators. As we move on to organic(6) molecules though, whether a molecule replicates or not is not so clear. First, we are not talking about a reaction which is completed all in one step. As mentioned in the first paragraphs, such a molecule can accumulate pieces of “scrap” (smaller molecules) on its body in several steps (several reactions), growing in size. This growing makes it unstable, until at some point the internal bonds that hold its atoms together break, and several pieces result out of this final reaction. Now, there might be some pieces (more than one) that look a bit like the original molecule that started this series of reactions. How much any of those pieces looks like the original, determines how good a replicator the original molecule is. “Looking alike” is not a true-or-false property.
The program presented earlier on this page starts with a replicator that is not good at replicating at all: very soon after it appears it mutates to other types, which may or may not be replicators. Only the few decendants which, by chance, happen to be even better replicators will keep and in fact improve the "replicating" character, and the best of them will produce viable populations. This is why, if you let the program run for awhile, the original purple hue soon gets replaced by different ones.
What do we know about such possibly-replicating-but-not-quite molecules? Not much, yet. No biologist, or chemist, has so far succeeded in proposing a molecule, other than our familiar DNA and its ken, which can be characterized as a replicator,(7) of the kind that would lead to terrestrial life. Why would we be interested in a molecule other than DNA? Because the DNA is already fairly complex, and we assume that itself is the product of evolutionary change. DNA, together with its counterpart, RNA, are probably the lone survivors of a long history of “struggle for survival” among replicators and near-replicators. How do we know this? DNA and RNA cannot replicate by themselves. They require the existence of certain proteins in their environment. However, those proteins can only be manufactured in the presence of molecules such as DNA and RNA. Here we have a chicken-and-egg problem: neither DNA, nor the proteins could have appeared first, because the one requires the other. The only possible answer to this problem is that what we observe today is the end-product of a long chain of changes. In the beginning of this chain must have been molecules that replicated in the simple way that I outlined earlier (accumulating, growing, splitting). Somewhere along this chain there appeared substances that started “cooperating” with each other, not because they “wanted” it, but because this cooperation resulted in more viable populations, hence the cooperating character persisted. The evolutionary end-product of such cooperating couples is DNA and the proteins. By the way, cooperation is not something unique to this case. It appears over and over again as a theme in biology. Each one of us lives because of such cooperation, too: mammals, including people, have certain bacteria in their intestines that help in digestion. Bacteria are complete and usually autonomous organisms, and although invisible to the unaided eye, they are as valid “living beings” as any other. If such bacteria were removed from our intestines, we would die. But those bacteria, too, cannot live anywhere else but in our intestines. We thus have a simple example of cooperation between organisms here, one which is called symbiosis. Probably the most primitive known example of symbiosis is the DNA-proteins pair. Whatever has existed prior to this end-product must have been significantly simpler. Still, it was evidently complex enough to escape identification by contemporary science. There is a reason for this: on the one hand, the majority of biologists do not work on the subject of the origins of life.(8) On the other hand, the majority of chemists and molecular biologists — who are better suited in pursuing the discovery of replicator molecules — are not interested so much in the beginnings of life either, which they regard as rather remote from what is commercially useful today. So there is only a small number of scientists who work directly in this area. Only time can make up for the insufficient scientific activity on this subject.
Why don’t we see replicator molecules being produced spontaneously today, if this was possible four billion years ago? Because the necessary conditions that existed in a primordial Earth, when the relevant reactions were taking place, are not in existence today: the present terrestrial environment is vastly different, so it doesn’t support the (re-)birth of life. Neither was the environment four billion years ago supportive of the present forms of life. Suffice it to say that if we could somehow miraculously be transported on the surface of our planet at that time, we would die of asphyxiation. Living organisms have modified drastically the earthly environment; as a result, what was possible four billion years ago is not possible now.(9) Besides, even if a chemical reaction takes place today that leads to potentially replicating molecules — somewhere in the vastness of our planet’s environment, away from curious scientific eyes — it is very likely that the resulting would-be-replicators become a nice meal for those who have already mastered and perfected the replicating art: the bacteria. The “replicating niche”, or, in other words, the “super-niche of biology” on this planet is already taken.
Footnotes (Clicking on the footnote number, on the left, brings back to the text. )
 It was brought to my attention that some cases of animals committing suicide might exist. For example, dogs or cats letting themselves die after the death of their owners; or dolphins, committing suicide in captivity (see this page). Such cases are possible, and show that the line that separates psychology from biology is not a hard and crisp one, separating our species from the rest of the animal kingdom. Other cases, however, such as bees dying to protect their hive, lionesses dying to protect their young, etc., are all explicable with reference to the idea that what matters is the propagation of genes, not the survival of the individual — a point that will be further explained later.
 We already know at least one self-replicating molecule: it is the DNA (or rather, the DNA + proteins — please read further in the text). So there is no doubt about whether a replicator molecule can ever exist. The DNA, however, cannot be the very first replicator molecule that existed, because it is already quite complex. To see how simpler replicators may have emerged on Earth, please read further in this text. (If you want to go there now, click here.)
 If you’re looking at the code of this program, check methods PhenotypeFromGenotype(), and React(), in Molecule.java. If you are a programmer, feel free to “mutate” the code in any way you like, adding your own copyright comment and retaining the original one(s) as a courtesy to the original author(s).
 Notice that here I use the word mutation as a synonym for gene. Although this is incorrect, it is unreasonable to expect that the earliest replicators which we refer to in this text would have employed genes (collections of molecules “coding for” properties of an organism) as we know them. So I’ll keep using the word “mutation” to refer to an imperfect copy of the original replicator.
 I am aware of the fact that religions such as Christianity, Islam, and Judaism, teach that our “souls” keep existing after the death of the body, and thus, according to them, God has actually seen it that we, human beings, live forever. Another point of view, which I espouse, says that such beliefs are the natural reaction of a creature (humans) who was the first and only one to have the cognitive ability to project the present into the future, conclude that death is unavoidable, be scared of it, and develop various cognitive defenses against this fear. The most effective such defense seems to be the belief that some part of ourselves keeps living after death. Such beliefs are understandable, but, in my view, ultimately baseless: there is nothing in the real world that supports them, save for our own fears. I am of the opinion that a better understanding of the real world in which we live helps in alleviating such fears, giving us a proper perspective of our place in the cosmos. My personal beliefs on religion and its origins are better explained in this page.
 “Organic” means simply that the molecule contains one or more atoms of carbon.
 This is not entirely true. In 1861, the Russian chemist Alexander Butlerov described the formose reaction, in which a solution of formaldehyde and sugars (both simple organic compounds) results in the multiplication of the sugars at an accelerating rate, in a process known as autocatalysis. More recently, in 1986, the first artificial replicator not needing enzymes for its replication was synthesized by K. von Kiedrowski.
 It’s not because they don’t like the subject, but because there is a large gamut of interesting topics in biology, all of which are actively explored.
 The same explanation applies to every instance of evolutionary change: no species may “reappear” as the product of evolution because the conditions that led to its emergence were unique, in every case — since environmental conditions are at a constant flux and never repeat themselves down to the last detail.
Richard Dawkins, The Selfish Gene. Oxford University Press, Oxford 1976.
Richard Dawkins, The Blind Watchmaker. W. W. Norton & Company, New York 1987.
Daniel Dennett, Darwin's Dangerous Idea. Penguin Press, London 1995.
Scott Freeman and Jon C. Herron, Evolutionary Analysis. Prentice Hall, NJ 2001.
John Maynard Smith and Eörs Szathmáry, The Origins of Life. Oxford University Press, Oxford 1999.
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Created: February 2002. Last modified: October 2008