The Surprising Origins of Life’s Complexity

Scientists are exploring how organisms can evolve elaborate structures without Darwinian selection.

The human eye evolved gradually, with natural selection favoring intermediate forms, but studies indicate that complexity may also emerge by other means.

Suren Manvelyan

The human eye evolved gradually, with natural selection favoring intermediate forms, but studies indicate that complexity may also emerge by other means.

Charles Darwin was not yet 30 when he got the basic idea for the theory of evolution. But it wasn’t until he turned 50 that he presented his argument to the world. He spent those two decades methodically compiling evidence for his theory and coming up with responses to every skeptical counterargument he could think of. And the counterargument he anticipated most of all was that the gradual evolutionary process he envisioned could not produce certain complex structures.

Consider the human eye. It is made up of many parts—a retina, a lens, muscles, jelly, and so on—all of which must interact for sight to occur. Damage one part—detach the retina, for instance—and blindness can follow. In fact, the eye functions only if the parts are of the right size and shape to work with one another. If Darwin was right, then the complex eye had evolved from simple precursors. In On the Origin of Species, Darwin wrote that this idea “seems, I freely confess, absurd in the highest possible degree.”

But Darwin could nonetheless see a path to the evolution of complexity. In each generation, individuals varied in their traits. Some variations increased their survival and allowed them to have more offspring. Over generations those advantageous variations would become more common—would, in a word, be “selected.” As new variations emerged and spread, they could gradually tinker with anatomy, producing complex structures.

In Brief

Conventional wisdom holds that complex structures evolve from simpler ones, step-by-step, through a gradual evolutionary process, with Darwinian selection favoring intermediate forms along the way.

But recently some scholars have proposed that complexity can arise by other means—as a side effect, for instance—even without natural selection to promote it.

Studies suggest that random mutations that individually have no effect on an organism can fuel the emergence of complexity in a process known as constructive neutral evolution.

The human eye, Darwin argued, could have evolved from a simple light-catching patch of tissue of the kind that animals such as flatworms grow today. Natural selection could have turned the patch into a cup that could detect the direction of the light. Then, some added feature would work with the cup to further improve vision, better adapting an organism to its surroundings, and so this intermediate precursor of an eye would be passed down to future generations. And, step-by-step, natural selection could drive this transformation to increased complexity because each intermediate form would provide an ad–vantage over what came before.

Darwin’s musings on the origin of complexity have found support in modern biology. Today biologists can probe the eye and other organs in detail at the molecular level, where they find immensely complex proteins joining together to make structures that bear a striking resemblance to portals, conveyor belts and motors. Such intricate systems of proteins can evolve from simpler ones, with natural selection favoring the intermediates along the way.

But recently some scientists and philosophers have suggested that complexity can arise through other routes. Some argue that life has a built-in tendency to become more complex over time. Others maintain that as random mutations arise, complexity emerges as a side effect, even without natural selection to help it along. Complexity, they say, is not purely the result of millions of years of fine-tuning through natural selection—the process that Richard Dawkins famously dubbed “the blind watchmaker.” To some extent, it just happens.

A Sum of Varied Parts

Biologists and philosophers have pondered the evolution of complexity for decades, but according to Daniel W. McShea, a paleobiologist at Duke University, they have been hobbled by vague definitions. “It’s not just that they don’t know how to put a number on it. They don’t know what they mean by the word,” McShea says.

McShea has been contemplating this question for years, working closely with Robert N. Brandon, also at Duke. McShea and Brandon suggest that we look not only at the sheer number of parts making up living things but at the types of parts. Our bodies are made of 10 trillion cells. If they were all of one type, we would be featureless heaps of protoplasm. Instead we have muscle cells, red blood cells, skin cells, and so on. Even a single organ can have many different cell types. The retina, for example, has about 60 different kinds of neurons, each with a distinct task. By this measure, we can say that we humans are, indeed, more complex than an animal such as a sponge, which has perhaps only six cell types.

One advantage of this definition is that you can measure complexity in many ways. Our skeletons have different types of bones, for example, each with a distinctive shape. Even the spine is made up of different types of parts, from the vertebrae in the neck that hold up our head to the ones that support our rib cage.

In their 2010 book Biology’s First Law, McShea and Brandon outlined a way that complexity defined in this way could arise. They argued that a bunch of parts that start out more or less the same should differentiate over time. Whenever organisms reproduce, one or more of their genes may mutate. And sometimes these mutations give rise to more types of parts. Once an organism has more parts, those units have an opportunity to become different. After a gene is accidentally copied, the duplicate may pick up mutations that the original does not share. Thus, if you start with a set of identical parts, according to McShea and Brandon, they will tend to become increasingly different from one another. In other words, the organism’s complexity will increase.

As complexity arises, it may help an organism survive better or have more offspring. If so, it will be favored by natural selection and spread through the population. Mammals, for example, smell by binding odor molecules to receptors on nerve endings in their nose. These receptor genes have repeatedly duplicated over millions of years. The new copies mutate, allowing mammals to smell a wider range of aromas. Animals that rely heavily on their nose, such as mice and dogs, have more than 1,000 of these receptor genes. On the other hand, complexity can be a burden. Mutations can change the shape of a neck vertebra, for instance, making it hard for the head to turn. Natural selection will keep these mutations from spreading through populations. That is, organisms born with those traits will tend to die before reproducing, thus taking the deleterious traits out of circulation when they go. In these cases, natural selection works against complexity.

Unlike standard evolutionary theory, McShea and Brandon see complexity increasing even in the absence of natural selection. This statement is, they maintain, a fundamental law of biology—perhaps its only one. They have dubbed it the zero-force evolutionary law.

The Fruit-Fly Test

Recently McShea and Leonore Fleming, a graduate student at Duke, put the zero-force evolutionary law to the test. The subjects were Drosophila flies. For more than a century scientists have reared stocks of the flies to use in experiments. In their laboratory homes, the flies have led a pampered life, provided with a constant supply of food and a steady, warm climate. Their wild relatives, meanwhile, have to contend with starvation, predators, cold and heat. Natural selection is strong among the wild flies, eliminating mutations that make flies unable to cope with their many challenges. In the sheltered environment of the labs, in contrast, natural selection is feeble.

Edward Kinsman

Lab-raised fruit flies are more complex than wild ones because their sheltered environment allows even disadvantageous mutations to spread. This mutant Drosophila has bar-shaped eyes that are smaller than normal.

The zero-force evolutionary law makes a clear prediction: over the past century the lab flies should have been less subject to the elimination of disadvantageous mutations and thus should have become more complex than the wild ones.

Fleming and McShea examined the scientific literature for 916 laboratory lines of flies. They made many different measures of complexity in each population. In the journal Evolution & Development, they recently reported that the lab flies were indeed more complex than wild ones.

Although some biologists have endorsed the zero-force evolutionary law, Douglas Erwin, a leading paleontologist at the Smithsonian National Museum of Natural History, thinks it has some serious flaws. “One of its basic assumptions fails,” he argues. According to the law, complexity may increase in the absence of selection. But that would be true only if organisms could actually exist beyond the influence of selection. In the real world, even when they are pampered by the most doting of scientists, Erwin contends, selection still exerts a force. For an animal such as a fly to develop properly, hundreds of genes have to interact in an elaborate choreography, turning one cell into many, giving rise to different organs, and so on. Mutations may disrupt that choreography, preventing the flies from becoming viable adults.

An organism can exist without external selection—without the environment determining who wins and loses in the evolutionary race—but it will still be subject to internal selection, which takes place within organisms. In their new study, McShea and Fleming do not provide evidence for the zero-force evolutionary law, according to Erwin, “because they only consider adult variants.” The researchers did not look at the mutants that died from developmental disorders before reaching maturity, despite being cared for by scientists.

Some of the insects had irregular legs. Others acquired complicated patterns of colors on their wings. The segments of their antennae took on different shapes. Freed from natural selection, flies have reveled in complexity.

Another objection Erwin and other critics have raised is that McShea and Brandon’s version of complexity does not jibe with how most people define the term. After all, an eye does not just have many different parts. Those parts also carry out a task together, and each one has a particular job to do. But McShea and Brandon argue that the kind of complexity that they are examining could lead to complexity of other sorts. “The kind of complexity that we’re seeing in this Drosophila population is the foundation for really interesting stuff that selection could get hold of” to build complex structures that function to aid survival, McShea says.

Molecular Complexity

As a paleobiologist, McShea is accustomed to thinking about the kind of complexity he can see in fossils—bones fitting together into a skeleton, for example. But in recent years a number of molecular biologists have independently begun to think much as he does about how complexity emerges.

In the 1990s a group of Canadian biologists started to ponder the fact that mutations often have no effect on an organism at all. These mutations are, in the jargon of evolutionary biology, neutral. The scientists, including Michael Gray of Dalhousie University in Halifax, proposed that the mutations could give rise to complex structures without going through a series of intermediates that are each selected for their help in adapting an organism to its environment. They dubbed this process “constructive neutral evolution.”

Gray has been encouraged by some recent studies that provide compelling evidence for constructive neutral evolution. One of the leaders in this research is Joe Thornton of the University of Oregon. He and his colleagues have found what appears to be an example in the cells of fungi. In fungi, such as a portobello mushroom, cells have to move atoms from one place to another to stay alive. One of the ways they do so is with molecular pumps called vacuolar ATPase complexes. A spinning ring of proteins shuttles atoms from one side of a membrane in the fungus to another. This ring is clearly a complex structure. It contains six protein molecules. Four of the molecules consist of the protein known as Vma3. The fifth is Vma11 and the sixth Vma16. All three types of protein are essential for the ring to spin.

Illustration courtesy of Nature

Scientists have proposed that complexity can sometimes evolve without the help of natural selection. Here’s an example of how this might occur. A: The gene A encodes a protein with a structure that allows eight copies of it to assemble into a ring. B: The gene accidentally duplicates. Initially, the two kinds of proteins can combine in any order to produce the same ring. C: Mutations take away some of the sites at which the proteins can bind. Now they can only arrange themselves in one particular combination. The ring has become more complex, but not because complexity was favored by natural selection.

To find out how this complex structure evolved, Thornton and his colleagues compared the proteins with related versions in other organisms, such as animals. (Fungi and animals share a common ancestor that lived around a billion years ago.)

In animals, the vacuolar ATPase complexes also have spinning rings made of six proteins. But those rings are different in one crucial way: instead of having three types of proteins in their rings, they have only two. Each animal ring is made up of five copies of Vma3 and one of Vma16. They have no Vma11. By McShea and Brandon’s definition of complexity, fungi are more complex than animals—at least when it comes to their vacuolar ATPase complexes.

The scientists looked closely at the genes encoding the ring proteins. Vma11, the ring protein unique to fungi, turns out to be a close relative of the Vma3 in both animals and fungi. The genes for Vma3 and Vma11 must therefore share a common ancestry. Thornton and his colleagues concluded that early in the evolution of fungi, an ancestral gene for ring proteins was accidentally duplicated. Those two copies then evolved into Vma3 and Vma11.

By comparing the differences in the genes for Vma3 and Vma11, Thornton and his colleagues reconstructed the ancestral gene from which they both evolved. They then used that DNA sequence to create a corresponding protein—in effect, resurrecting an 800-million-year-old protein. The scientists called this protein Anc.3-11—short for ancestor of Vma3 and Vma11. They wondered how the protein ring functioned with this ancestral protein. To find out, they inserted the gene for Anc.3-11 into the DNA of yeast. They also shut down its descendant genes, Vma3 and Vma11. Normally, shutting down the genes for the Vma3 and Vma11 proteins would be fatal because the yeast could no longer make their rings. But Thornton and his co-workers found that the yeast could survive with Anc.3-11 instead. It combined Anc.3-11 with Vma16 to make fully functional rings.

Illustration courtesy of Nature

University of Oregon scientists have reconstructed the evolution of a complex structure found in yeast and other fungi. Left: Yeast use a pump called vacuolar-ATPase to move charged proteins across their membranes. One key part of this pump is a ring made up of six interlocking proteins (shown in color here). Right: By comparing the ring in fungi to the ring in animals, the researchers have reconstructed its evolution. The ancestral ring had two types of protein. The black squares, triangles and circles show sites of the proteins that can bind to other proteins at sites marked with corresponding holes. In fungi, one of the genes duplicated, producing three types of proteins. Some of the proteins lost sites where other proteins could bind, marked here by red spots. This real-world example matches the scenario in the previous figure.

Experiments such as this one allowed the scientists to formulate a hypothesis for how the fungal ring became more complex. Fungi started out with rings made from only two proteins—the same ones found in animals like us. The proteins were versatile, able to bind to themselves or to their partners, joining up to proteins either on their right or on their left. Later the gene for Anc.3-11 duplicated into Vma3 and Vma11. These new proteins kept doing what the old ones had done: they assembled into rings for pumps. But over millions of generations of fungi, they began to mutate. Some of those mutations took away some of their versatility. Vma11, for example, lost the ability to bind to Vma3 on its clockwise side. Vma3 lost the ability to bind to Vma16 on its clockwise side. These mutations did not kill the yeast, because the proteins could still link together into a ring. They were neutral mutations, in other words. But now the ring had to be more complex because it could form successfully only if all three proteins were present and only if they arranged themselves in one pattern.

Thornton and his colleagues have uncovered precisely the kind of evolutionary episode predicted by the zero-force evolutionary law. Over time, life produced more parts—that is, more ring proteins. And then those extra parts began to diverge from one another. The fungi ended up with a more complex structure than their ancestors had. But it did not happen the way Darwin had imagined, with natural selection favoring a series of intermediate forms. Instead the fungal ring degenerated its way into complexity.

Fixing Mistakes

Gray has found another example of constructive neutral evolution in the way many species edit their genes. When cells need to make a given protein, they transcribe the DNA of its gene into RNA, the single-stranded counterpart of DNA, and then use special enzymes to replace certain RNA building blocks (called nucleotides) with other ones. RNA editing is essential to many species, including us—the unedited RNA molecules produce proteins that do not work. But there is also something decidedly odd about it. Why don’t we just have genes with the correct original sequence, making RNA editing unnecessary?

The scenario that Gray proposes for the evolution of RNA editing goes like this: an enzyme mutates so that it can latch onto RNA and change certain nucleotides. This enzyme does not harm the cell, nor does it help it—at least not at first. Doing no harm, it persists. Later a harmful mutation occurs in a gene. Fortunately, the cell already has the RNA-binding enzyme, which can compensate for this mutation by editing the RNA. It shields the cell from the harm of the mutation, allowing the mutation to get passed down to the next generation and spread throughout the population. The evolution of this RNA-editing enzyme and the mutation it fixed was not driven by natural selection, Gray argues. Instead this extra layer of complexity evolved on its own—“neutrally.” Then, once it became widespread, there was no way to get rid of it.

David Speijer, a biochemist at the University of Amsterdam, thinks that Gray and his colleagues have done biology a service with the idea of constructive neutral evolution, especially by challenging the notion that all complexity must be adaptive. But Speijer worries they may be pushing their argument too hard in some cases. On one hand, he thinks that the fungus pumps are a good example of constructive neutral evolution. “Everybody in their right mind would totally agree with it,” he says. In other cases, such as RNA editing, scientists should not, in his view, dismiss the possibility that natural selection was at work, even if the complexity seems useless.

Gray, McShea and Brandon acknowledge the important role of natural selection in the rise of the complexity that surrounds us, from the biochemistry that builds a feather to the photosynthetic factories inside the leaves of trees. Yet they hope their research will coax other biologists to think beyond natural selection and to see the possibility that random mutation can fuel the evolution of complexity on its own. “We don’t dismiss adaptation at all as part of that,” Gray says. “We just don’t think it explains everything.”

This article was produced in collaboration with Scientific American and printed in the August 2013 issue of the magazine.


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  • Carl,
    nifty riff :3

    Howard Bloom writes aboot this (among other things) in his book “The God Problem: How a Godless Cosmos Creates”

  • I have read that Herbert Spencer held to a very similar theory of a natural tendency towards complexity, and advanced it as the basis for evolution on every scale.

  • I think the distinction between adaptation driving the evolution of complexity versus a neutral ratchet toward complexity (as in the paper from Thornton’s group) might largely be semantic. If you consider the gene as the unit of selection, more complexity might be adaptive, in the sense that more interactions make it harder for other alleles to replace you. On the organismal level, such changes might be neutral, if the more complicated heteromer protein complex is just as good as the simpler homomer.

  • Other than giving new names and providing admittedly cool and interesting experimental evidence, I fail to see how this is any different from the classical view of evolution we have taught for the last few decades. The role of chance and neuetral evolution has always been a part of evolutionary theory and we have known for decades that adaptation did not explain everything, that some things happened just through randomness and were retained because it did not kill off the organism. That is the whole basis for how exaptations originate.

  • @Rohan Maddamsetti- looking at it from the perspective of Richard Dawkins’s Selfish Gene? Yeah, that makes sense.

  • I am still a bit confused about the definition of complexity. Why do we assume that a machine with three parts is more complex than a machine with two parts that does the same task. If we consider the functionality of the parts rather than the number of parts, wouldn’t the latter be more complex?

    Similarly with the RNA-editing. Why is the broken and then patched up mechanism more complex than the original, unbroken mechanism that has the ability to patch itself up?

  • Consider creatures with atrophied limbs – snakes, manatees, whales. In snakes, I can see that regardless of what led them to crawl on their ribs, legs may have been a hindrance and a selection factor. Assuming that’s true, if variation or mutation had not shrunken the legs then snakes would not be legless, or might be something else. This seems half-baked to me, particularly with whales – is it enough to say they are what they are (I understand I can’t say something else should have happened).

  • Complexity take time to produce, at least if you want a coordinated whole and not a jumble. On the other hand by creating a differentiated background field processes that might otherwise take a long time can be speeded up (as with enzymes). This means that there must be more than one parameter behind complexity. Even in our daily lives we see a similar effect. Planned preparation and assembly of all the requisite parts, etc. allows for a task to be performed relatively quickly. If the prior steps themselves are tasks coordinated by even further previous prep and assembly, and so on, then we can jump from one task to another. We don’t have to wait for the right conditions- everything is automatized. Context dependency is at a minimum. The split of DNA into regulatory ‘junk’ and protein-coding genes is interesting from this perspective because the former appears to correlate with high context dependency, giving the system choices as it reacts to different environmental conditions, including waiting for new information that may take a while to receive. The editable genes add another layer to such choice. At the other end of the spectrum we have bacterial genomes, which have little, if any ‘junk’ or editing. They are all business, knee-jerk machines. And yet interestingly we also have lateral gene transfer at a maximum, so that when encountering other organisms that have adapted to new (for the immigrant) environmental conditions it can improve its chances for survival through trade of meat-and-potatoes protein-coding genes . Eukaryotes, by contrast, depend more upon internal resources by and large but can also acquire new abilities to regulate their own genomes by being infected by viruses (which are essentially molecular executives) which become part of the ‘junk’. A difference of hierarchical level- eukaryotes prefer top- and mid-level hires, while prokaryotes do low-level ones.

  • My goodness the standards to which we hold Mr. Darwin, and find him wanting! I am half-joking, but the serious side of me is a little weary of statements like: “But it did not happen the way Darwin had imagined…” that fill otherwise wonderful pieces like this. It is a useful but worn hook to compare the new advances in a field with orders of magnitude more data to the theorizing of a gentleman naturalist more than 150 years ago. I suppose, in your defense, that it is the exceptions like these that prove the rule that “On the Origin…” was the single greatest work in the history of biology.

  • It sounds vaguely like the “hopeless monster” idea. But near neutral drift will also destroy what has been complexified just because it is random, unless it is fixated.

    So yes, renaming what is known sounds like what is going on. That can be bad, neutral, or beneficial depending on what ideas the new terms engender…

  • I see nothing wrong with this theory. If one discerns all of the possible mechanisms for growth and change of the genome one can determine to what extent each plays a role in the process of evolution. Exon shuffling, gene duplication, spontaneous mutations, epigenetics, symbiosis, and lots and lots of generations. Yet in the end evolution is merely about inevitability, and for that we can thank only the universal constants.

  • This kind of view has been bubbling up for decades now, but there is strong resistance from those who are too ‘in love’ with the idea of Darwinism (in my opinion). There is another book that was written in a very heretical tone, but which makes a strong case for this perspective, by Reid called “Biological Emergences”. I highly recommend this book, but be prepared for a curmudgeonly author who does not hold back his disdain for the ‘Darwinists’ who he thinks should have acknowledged this view long ago.

  • While sitting in a class half a century ago, I heard the professor expound on vitamin c and cockroaches. It seems that there are over a dozen enzymes required to synthesize vitamin c. The cockroach has them all and we, as humans, have all but one. This was presented as an example of a non fatal mutation that cost us the that ability. Non fatal in that we typically have enough vitamin c in our diet to prevent scurvy.

    Was there an “oops” in our past, or are we not there yet?

  • Physics Nobel prize winner and one of the founders of the Santa Fe Institute, New Mexico, (which studies the complexity), Murray Gell-Mann, wrote in 1996 in his book „The Quark and the Jaguar“: „Any definition of complexity is necessarily context-dependent, even subjective.“
    And as Jack Cohen & Ian Stewart wrote in their book “The collapse of chaos” : “This phenomenon – of vastly complex effects arising from simple causes – is known as chaos, and there is plenty of evidence that it is widespread.”

  • Evolution = random mutation + natural selection. Setting aside natural selection, random mutation is simply nature’s adherence to DeMorgan’s Law: “If something can happen it will happen”; well illustrated by “The Infinite Monkey theorem”: given enough time, a monkey randomly hitting keys on a typewriter will produce “War and Peace”. Since the mutations are “random” simplicity/complexity aren’t qualifiers.

  • Something seems to have gone wrong here. Why are we looking at “complexity” per se? Darwin was not *primarily* concerned to explain complexity but evolutionary change and specifically *adaptative* evolutionary change. One can imagine an eye that has Rube-Goldberg-like “complexity”–much more complexity than the actual eye–but so what?

    The whole context for understanding living organisms is . . . well . . . life. Survival value (or reproductive fitness) is the *ultimate* explanation of everything about organisms–why they are complex when they are, why they get simplified (like intestinal flora and fauna) when they do, why they have this structure rather than that.

    Doesn’t “neutral constructive complexity” provide, at most, the raw material upon which natural selection than operates?

  • “Complexity” has simply been conflated with “variation” in the definition put forth by McShea and Brandon. Evolutionary theory already accounts for variation in populations — i.e. the wide range of options that random mutations churn out. Natural selection, only one facet of evolutionary theory, is just the natural outcomes of those variants where options that don’t work, don’t usually stick around long enough to reproduce. Variation in a population should not be confused with complexity.

  • RNA: the authors’ scenario doesn’t make sense. It doesn’t explain why a harmful-mutation-with-the-RNA-fix would evolve in place of the original DNA copying process:

    “an enzyme mutates so that it can latch onto RNA and change certain nucleotides. This enzyme does not harm the cell, nor does it help it—at least not at first. Doing no harm, it persists. Later a harmful mutation occurs in a gene. Fortunately, the cell already has the RNA-binding enzyme, which can compensate for this mutation by editing the RNA. It shields the cell from the harm of the mutation, allowing the mutation to get passed down to the next generation and spread throughout the population. The evolution of this RNA-editing enzyme and the mutation it fixed was not driven by natural selection, Gray argues. Instead this extra layer of complexity evolved on its own—“neutrally.” Then, once it became widespread, there was no way to get rid of it.””

    Why would it become widespread in the first place? Why would that error-then-RNA-fix reproduce more than the original non-mutated DNA copy system? If there was this harmful mutation in ONE single organism that just happened to be saved by the fortuitously placed RNA mutation, that mutation would simply make the organism less efficient at copying DNA than an organism that had not suffered the same mutation. The error-then-RNA-fix would therefore die on the vine if it were still competing with organisms that DID NOT suffer the harmful mutation.

  • I am curious if these neutral mutations generate more total entropy than their predecessors did.
    I think you already see where i am going to go but if not I will try to explain. So i had this thought when i was reading the article: “what if the random mutations are not so much as random as they are necessary for satisfying the universes tendency towards maximum entropy”. I stress that I have no idea if the mutations generate more or less or the same amount of entropy as the ones before them but i think it is worth investigating just for the sake of knowing it.
    Just wanted to throw this out there.
    Good day.

  • life is a competition between different sorts of structures or bio-shapes, that we call living being, why there is not only one sort of bio-shape ? the amazing diversity is not very “natural”, don’t you think so ? if that have an adaptative purpose, so how nature knows that ? if not otherwise, what is the purpose of life in general, some says organisms are a natural evolution of inanimate matter, a more powerfull way to disperse energy, that may be a relevant new way of thinking evolution, science will improve, we have to stay vigilant

  • I am Reading this article quite late the day gravitational waved have been discovered by LIGO. And I rebound on previous comment.
    Let's admit that purpose of life is to "disperse energy" and even, in no contradiction to the second principle, to actually bring more entropy to the universe.
    What does today bring the more energy? A Star.
    So purpose of life is to be able to create more energy than a star.
    How to do that? Back to the LIGO story of the collapse of two black holes.
    Fist create or gather one star. then create or gather several stars. Then make them collapse to a black hole. Not enough? Make two black holes and make them collapse onto each other!
    You have created quite a massive event able to generate massive gravitational waves. (in the LIGO detection the collapse of 2 black holes of 30 solar masses has converted to energy 3 solar masses in a "blink of an eye". It sounds like a good way to "burn fuel".)
    Not enough, it is still natural ? Control this process. Aim is to master the process so that you can actually shape the space/time fabric at your will!
    Sounds like SF? it is SF!

    Dyson sphere and Star Wars idea to get energy from stars are nice but unsufficient to justify life.
    If life is to be justified by entropy it must create more entropy than a star, or a black hole or even two black holes fusioning.
    So life is to be a little more ambitious than just mastering nuclear fusion or getting star energy. It needs to go orders of magnitude beyond nuclear fusion energy. Mastering the use of black holes and space-time fabric has some potential.

  • "To some extent, it just happens." How utterly disappointing an explanation this is. Why not try to uncover the mysteries of how life evolved and use this knowledge to create and build. Thats like saying any engineered product 'to some extent, just happens.' Why sell yourself and science in general so short? What a joke.

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