Darwinism

How Darwinism is changing medicine

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A laboratory technician screens cancer samples (Credit: Getty Images)

The relatively new discipline of evolutionary medicine is making strides in the fields of cancer treatment and antibacterial resistance.

At age 20, Randolph Nesse was puzzled about why we grow old. He couldn’t wrap his head around why natural selection had not eliminated ageing altogether. He spent months coming up with theories to explain it, but was unable to solve the riddle. Yet, this idling of his inquiring mind would lay the seeds for a whole new way of thinking about medicine.

Some years later, friends at a local natural history museum pointed Nesse towards the theory that ageing is simply a side effect of the evolutionary pressure that has selected certain genes over others. If a condition only manifests after an organism passes its reproductive peak, then there will be no selective pressure to prevent it from being passed on. As a physician, Nesse realised that while he understood how these forces could shape species, he had no clue how natural selection works inside the human body.

“I learned one half of biology. Nobody had ever talked about the relevance of evolutionary biology [in medicine],” says Nesse. “I immediately started wondering if there were similar explanations for genes that cause disease.”

Nesse is now credited as a founding father of evolutionary medicine, sometimes also known as Darwinian medicine – a relatively new and growing discipline that applies evolutionary theory to questions about human health and disease. While most modern medical research focuses on the physical and molecular causes of disease, evolutionary medicine tries to understand why we might have evolved to be susceptible to conditions in the first place, and how we can use evolution to fight them.

“What we’re dealing with here is a whole new basic science that has not been applied to medicine,” Nesse says. It’s a very large enterprise to completely upend what we think about what the human body is and how it works. Yet, a growing number of scientists are trying to apply evolutionary thinking to improve medicine. Their work is already starting to change our understanding of how cancers and autoimmune diseases develop. It is also revealing new strategies for tackling pernicious healthcare-related problems such as antimicrobial resistance.

“I’ve been amazed that there have been so many practical implications so quickly,” says Nesse.Even the most powerful chemotherapy drugs are only effective for so long before cells develop resistance to them (Credit: Getty Images)

Even the most powerful chemotherapy drugs are only effective for so long before cells develop resistance to them (Credit: Getty Images)

Cancers are themselves a demonstration of the evolutionary process in a microcosm. They are clusters of cells that are continually competing and cooperating with each other in ways that help the tumour grow and flourish. One recent study highlighted the almost “infinite” ability of cancer cells to evolve and survive. When a patient receives drug therapy, for example, it introduces a new selective pressure that weeds out the cells that are most vulnerable to the treatment. Those that are less vulnerable, or even immune from the effects of the treatment, survive to pass on their genetic traits to the cells that follow them. It is why even highly successful cancer therapies will eventually stop working in many patients – the cancer cells develop resistance to the treatment and then uncontrollably grow their populations. 

“It is arguable that this is the proximate cause of death in most patients,” says Robert Gatenby, the co-director of the Center of Excellence for Evolutionary Therapy at Moffitt Cancer Center, in Florida, US. Through the lens of evolutionary thinking, Gatenby’s laboratory is developing two different strategies to tackle cancer: adaptive therapy, and extinction therapy.

Adaptive therapy aims to control cancer spread rather than try to eliminate it completely. The dogma for the last 50 years in cancer treatment has been that you apply the same drug, or combination of drugs, in cycles, until there is clear evidence of tumour progression (where the tumour begins growing uncontrollably) or excess toxicity, says Gatenby – which is usually well after the maximum response has been obtained. This is “futile”, he says, since the majority of the cells left are resistant to the drug and by continuing with the same therapy, the oncologist gives them the opportunity to proliferate so their population gets larger and more diverse. His theory of adaptive therapy, by contrast, aims to tweak the dosage of drugs for a tailored approach, just giving enough treatment to knock the tumour down, keeping it as small as possible, without eliminating the sensitive population completely. Then the therapy is withdrawn. This allows the cells sensitive to treatment to continue jostling for space within the tumour, preventing other drug-resistant cells from dominating due to an adaptive advantage.

“Since we can’t control the tumour cells that are resistant to therapy, we need to recruit the treatment-sensitive cells to do it for us,” says Gatenby, who has been developing the idea since first publishing on it in 1991. “You can just keep treating it in cycles and just keep knocking it down and letting it grow, knocking it down, letting it grow.” The hope, he says, is that doctors can keep patients alive for a long period of time, about half of which they don’t have to deal with the side-effects associated with the treatment.

His research group, which is arguably the most advanced in the field, have already shown this technique works in a small pilot trial involving patients with prostate cancer. Patients who underwent adaptive therapy received half the normal dose of a chemotherapy drug over the course of the trial, during which they spent 46% of the time receiving none at all. The time from starting the therapy to when the cancer stopped responding to treatment was 19 months longer in the group who received this adaptive therapy compared to those who underwent the standard course of chemotherapy. The patients who had adaptive therapy also had an overall survival that was 2.26 years greater than those on the standard treatment.

“As these patients only had about half the drug they would have received otherwise, the cost of their therapy was also $70,000 (£57,000) less per patient per year,” says Gatenby.

Our idea is maybe instead of an antibiotic being useful for 20 years, maybe it will become useful for 40 or 50 years – Anne Farewell

In extinction therapy, Gatenby wants to take it even a step further and use what we know from how animal species go extinct to design curative therapies that cause the extinction of cancer populations. The idea would be not to wait for the tumour to regrow after doctors apply the initial therapy, but rather, hitting the tumour with an altogether different therapy before it can recover – catching the tumour cells by surprise with a rapid cycle of a different drug at the peak of its response to that first-line treatment. So far though, only a mathematical model has been published to explore this idea, although Gatenby’s team has proposed clinical trials using extinction therapy against pancreatic cancer and breast cancer.

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The elephant in the room, in fact, is still how research like this is going to go from clinical trials, if it is successful, to acceptance in the real world, according to Michael E Hochberg, distinguished research director at the Centre National de la Recherche Scientifique of the University of Montpellier, in France. 

“The main part of the puzzle is turning this into medicine,” says Hochberg. “What is its realistic use, in terms of utility?”

Maybe evolutionary medicine really is the most likely scientific perspective on dealing with big questions like these, according to Hochberg, but doctors still have to treat patients every day by working with solutions they know, tried-and-tested best practices, and little room for hypotheses. “They have a duty to ‘first do no harm’,” he says, and right now, these findings are still too preliminary.

“I think that’s sort of the unspoken major critique of this,” says Hochberg. “Will this ever see the light of day?”Tumours are actually communities of cells that compete and cooperate with each other (Credit: Getty Images)

Tumours are actually communities of cells that compete and cooperate with each other (Credit: Getty Images)

Evolutionary medicine is also applied in the search for a solution to one of the fastest-growing problems of the modern world: antibacterial resistance. 

As modern medicine has developed powerful antibiotics to annihilate harmful bacteria that infect humans and causes diseases, their widespread use has also inadvertently led bacteria to evolve through natural selection resistance to these drugs. It is estimated that antimicrobial resistant bacteria killed more people than HIV/Aids or malaria in 2019, taking more than 1.2 million lives.

Currently, doctors combat diseases caused by antimicrobial-resistant bacteria by switching to other medications in the hope they will get around the bacterial defences against other drugs. But this practice risks continuing the cycle of resistance rather than stopping it – in fact, bacteria are evolving to become more and more genetically resistant to medication.

Bacteria also develop resistance in a whole range of ways – from swapping genetic material to accumulating random mutations. As a result, evolutionary scientists are testing various different approaches to break down these pathways.

“If we want to solve this problem, we need to understand the evolution and then go after the weak points,” says Andrew Read, the director of the Huck Institutes of the Life Sciences at Penn State University. Read’s team is developing “anti-antibiotic drugs” to help control the spread of antimicrobial resistance in places where the drugs can do more harm than good.

In hospitals, antimicrobial resistance usually happens because some of the strong antibiotics that patients get intravenously – about 5-10%, according to Read – make their way through to the patient’s digestive system. There, they meet an extensive community of microbes, causing harmful changes in the balance of that community and leaving some that have acquired antibiotic resistance. This is what happens in the case of diseases like Clostridium difficile (C. diff), where a patient’s gut is ravaged by this bacteria after having been treated with antibiotics for something else. If patients could take anti-antibiotics that null the effect of the drugs once they reach the gut, it would reduce the likelihood of bacteria there developing resistance. The inactivation drugs themselves don’t do anything, clinically, but they stop the drug from acting in the gut. 

“What I like about this approach is, it doesn’t matter at all about the resistance mechanism. It doesn’t matter if resistance is there,” says Read. “It doesn’t matter if and how it was acquired, it just stops the force that drives any resistance up in the population.”

Adaptive therapy approaches in cancer, for example, will require changing the way we think about these diseases – for instance, letting go of the war-like terminology, such as the “battle” and “fight” to “destroy” cancer

His laboratory has already shown this mechanism works well in mice to prevent the spread of the superbug Enterococcus faecium after antibiotic treatment. Other researchers have been able to show that some compounds, like a charcoal-based adsorbent or an enzyme called ribaxamase, can help avoid the spread of C. diff in mice through the same technique.

But this is a general solution that doesn’t inhibit resistance should bacteria and drugs meet.

One reason why bacterial resistance is so hard to tackle is that it doesn’t just happen through the typical, chance-driven evolutionary route – when a random mutation makes some bacteria stronger and able to resist medication. It also happens thanks to horizontal gene transfer, where loops of DNA called plasmids can be passed directly from one bacteria to another. This has been found to happen both within the same species of bacteria and between species. This process allows mutations that convey drug resistance to spread far more quickly.

Anne Farewell‘s research group at the University of Gothenburg, Sweden, is trying to slow down one of the mechanisms that bacteria use to share DNA horizontally, known as “conjugation“. It’s a kind of bacterial sex, where cells come into direct contact, often via a tube that runs between them.

“I know we can’t beat them,” says Farewell, a senior lecturer in molecular biology. “But our idea is maybe instead of an antibiotic being useful for 20 years, maybe it will become useful for 40 or 50 years.”

She’s screening large swathes of microbes to pinpoint which exact pairs of bacterial species can mix and match to mate through conjugation. She’s also researching whether there are any specific environmental conditions – like pesticides or heavy metal contamination – that make it easier, or harder, for those bacteria to conjugate.

Her research has already shown that Escherichia coli, a common bacteria that can cause food poisoning and a wide range of other infections, might be blocked from conjugating if it comes in contact with copper, which reduces its ability to conjugate by almost 100 times. Similarly, earlier research suggests that a certain class of synthetic fatty-acids could inhibit conjugation, as could even sage essential oil. Studies have found the same anti-conjugation properties in benzyl isothiocyanate, an antibacterial compound found in plants of the mustard family, and some naturally occurring chemicals called tanzawaic acids.  

“Understanding which molecules screw up conjugation could help develop effective ‘anti-conjugation drugs’, but research here is still preliminary, and there are still plenty of other ways DNA can be shared between bacteria that this approach won’t affect,” admits Farewell. Bacteria are incredibly savvy, she says. “I don’t think there’s going to be one solution. There will be many approaches.”Interrupting the transfer of genes between bacteria through conjugation might help to combat the spread of antibiotic resistance (Credit: Getty Images)

Interrupting the transfer of genes between bacteria through conjugation might help to combat the spread of antibiotic resistance (Credit: Getty Images)

While the fields of cancer research and bacterial resistance are the most advanced in the field of evolutionary medicine, there’s still a long way to go. Critics argue that despite understanding more about the theory of evolutionary medicine, it’s unclear to what extent this new knowledge can be used practically.

“The problem, in my personal opinion, is unbridled enthusiasm about this,” says Hochberg, who also recently penned a commentary piece on evolutionary medicine for the journal Frontiers. “I’ve rarely seen talks that really focus on this on the problem of the logistics, the profits, and the so forth of the transfer from the bench to the clinic,” he says. “That’s a whole different can of worms.”

Plus, there’s intellectual friction too. While Darwinian academics might be over-enthusiastic, the receiving end of these new theories tends to be more skeptical. Evolutionary medicine alone cannot cure anybody – it’s a framework for thinking about problems in medicine.

“Medicine is practiced by people who do not have training typically in anything to do with evolutionary biology,” says Bernard Crespi, an evolutionary biologist at Simon Fraser University who also recently wrote about the limitations of evolutionary medicine. “The main challenge is bridging the gap between the academics, the training of physicians, and the mindset of the physician in the context of the whole medical establishment of big drug companies.”

Gatenby believes that adaptive therapy approaches in cancer, for example, will require changing the way we think about these diseases – for instance, letting go of much of the war-like terminology, such as the “battle” and “fight” to “destroy” cancer – and thinking about management instead. It will take a lot of convincing, says Gatenby.

How evolutionary medicine is going to find a way to collaborate with the pharmaceutical industry is also still a big question mark.

But Nesse – the man who kickstarted it all – says evolutionary medicine still has the power to provide new questions and new answers about disease. “You can tell I get a little passionate about this because it’s ridiculous. There’s this gulf between evolutionary biology and medicine, and it’s actually harming human health,” Nesse says. “It’s a slow process, but science always wins.” 

The Octopus Genome: Not “Alien” but Still a Big Problem for Darwinism

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AMI_-_Oktopusvase.jpg

 These days, new genomes of different types of organisms are being sequenced and published on a regular basis. When some new genome is sequenced, evolutionary biologists expect that it will be highly similar to the genomes of other organisms that are assumed to be closely related.

As ENV already noted, the latest organism to have its genome sequenced has confounded that expectation: the octopus, whose genome was recently reported in Nature. It turns out to be so unlike other mollusks and other invertebrates that it’s being called “alien” by the scientists who worked on that project.

One article on the subject was titled “Don’t freak out, but scientists think octopuses ‘might be aliens’ after DNA study“:

Not to send you into a meltdown or anything but octopuses are basically ‘aliens’ — according to scientists.Researchers have found a new map of the octopus genetic code that is so strange that it could be actually be an “alien”.

[…]

“The octopus appears to be utterly different from all other animals, even other molluscs, with its eight prehensile arms, its large brain and its clever problem-solving abilities,” said US researcher Dr Clifton Ragsdale, from the University of Chicago.

[…]

Analysis of 12 different tissues revealed hundreds of octopus-specific genes found in no other animal, many of them highly active in structures such as the brain, skin and suckers.

Obviously no one thinks the octopus is an “alien” from another planet. (Nature News quotes one co-author of the paper on the genome noting that the alien quip is a “joke.”) But it certainly is alien to standard evolutionary expectations that genomes of related species ought to be highly similar. Thus, Nature points out the large number of unique genes found in the octopus genome:

Surprisingly, the octopus genome turned out to be almost as large as a human’s and to contain a greater number of protein-coding genes — some 33,000, compared with fewer than 25,000 in Homo sapiens.This excess results mostly from the expansion of a few specific gene families, Ragsdale says. One of the most remarkable gene groups is the protocadherins, which regulate the development of neurons and the short-range interactions between them. The octopus has 168 of these genes — more than twice as many as mammals. This resonates with the creature’s unusually large brain and the organ’s even-stranger anatomy. …

A gene family that is involved in development, the zinc-finger transcription factors, is also highly expanded in octopuses. At around 1,800 genes, it is the second-largest gene family to be discovered in an animal, after the elephant’s 2,000 olfactory-receptor genes.

The analysis also turned up hundreds of other genes that are specific to the octopus and highly expressed in particular tissues. The suckers, for example, express a curious set of genes that are similar to those that encode receptors for the neurotransmitter acetylcholine. The genes seem to enable the octopus’s remarkable ability to taste with its suckers.

Scientists identified six genes for proteins called reflectins, which are expressed in an octopus’s skin. These alter the way light reflects from the octopus, giving the appearance of a different colour — one of several ways that an octopus can disguise itself, along with changing its texture, pattern or brightness.

The technical paper explains that the octopus genome reveals “massive expansions in two gene families previously thought to be uniquely enlarged in vertebrates: the protocadherins, which regulate neuronal development, and the C2H2 superfamily of zinc-finger transcription factors.” Moreover:

We identified hundreds of cephalopod-specific genes, many of which showed elevated expression levels in such specialized structures as the skin, the suckers and the nervous system.

They conclude: “Our analysis suggests that substantial expansion of a handful of gene families, along with extensive remodelling of genome linkage and repetitive content, played a critical role in the evolution of cephalopod morphological innovations, including their large and complex nervous systems.” In other words, the cephalopod genome is unusual in many major respects, unlike other organisms we’ve sequenced.Actually, that’s not completely correct. There are some peculiar similarities between the cephalopod genome and something else they’ve seen — but they aren’t the kind of similarities that were predicted by common descent. The technical papers notes that the cephalopod genome bears unexpected resemblance in certain respects to vertebrate genomes — and since these similarities aren’t predicted by common descent, they predictably attribute them to convergent evolution:

the independent expansions and nervous system enrichment of protocadherins in coleoid cephalopods and vertebrates offers a striking example of convergent evolution between these clades at the molecular level.

Indeed, even within cephalopods they found evidence of convergent evolution (i.e., genetic similarity that didn’t fit the expectations of common descent): “Surprisingly, our phylogenetic analyses suggest that the squid and octopus protocadherin arrays arose independently. Unlinked octopus protocadherins appear to have expanded ~135 Mya, after octopuses diverged from squid.”But the big story here is the large number of unique genes found in the octopus genome. The technical paper elaborates on one of these major gene groups:

The octopus genome encodes 168 multi-exonic protocadherin genes, nearly three-quarters of which are found in tandem clusters on the genome (Fig. 2b), a striking expansion relative to the 17-25 genes found in Lottia [a limpet], Crassostrea gigas (oyster) and Capitella [polychaete worm, and annelid] genomes.

The paper doesn’t even try to speculate about how these unique cephalopod genes might have arisen. The standard view — that new genes originate via gene duplication — is hardly mentioned. But invoking gene duplication requires one to find another gene elsewhere that’s similar. Given that cephalopods apparently have many unique genes not similar to genes found in other organisms, gene duplication might not be a candidate explanation in many of these cases. One wonders if future investigators will resort to “de novo” gene origin.What’s that? Stephen Meyer explains in Darwin’s Doubt:

Remember: ORFans, by definition, have no homologs. These genes are unique — one of a kind — a fact tacitly acknowledged by the increasing number of evolutionary biologists who attempt to “explain” the origin of such genes through de novo (“out of nowhere”) origination.[…]

Many other papers invoke de novo origination of genes. Long mentions, for example, a study seeking to explain the origin of an antifreeze protein in an Antarctic fish that cites “de novo amplification of a short DNA sequence to spawn a novel protein with a new function.” Likewise, Long cites an article in Science to explain the origin of two human genes involved in neurodevelopment that appealed to “de novo generation of building blocks — single genes or gene segments coding for protein domains,” where an exon spontaneously “originated from a unique noncoding sequence.” Other papers make similar appeals. A paper in 2009 reported “the de novo origin of at least three human protein- coding genes since the divergence with chimp[s],” where each of them “has no proteincoding homologs in any other genome.” An even more recent paper in PLoS Genetics reported “60 new protein- coding genes that originated de novo on the human lineage since divergence from the chimpanzee,” a finding that was called “a lot higher than a previous, admittedly conservative, estimate.”

Another 2009 paper in the journal Genome Research was appropriately titled “Darwinian Alchemy: Human Genes from Noncoding RNA.” It investigated the de novo origin of genes and acknowledged, “The emergence of complete, functional genes — with promoters, open reading frames (ORFs), and functional proteins — from ‘junk’ DNA would seem highly improbable, almost like the elusive transmutation of lead into gold that was sought by medieval alchemists.” Nonetheless, the article asserted without saying how that: “evolution by natural selection can forge completely new functional elements from apparently nonfunctional DNA — the process by which molecular evolution turns lead into gold.”

The presence of unique gene sequences forces researchers to invoke de novo origin of genes more often than they would like. After one study of fruit flies reported that “as many as ~12% of newly emerged genes in the Drosophila melanogaster subgroup may have arisen de novo from noncoding DNA,” the author went on to acknowledge that invoking this “mechanism” poses a severe problem for evolutionary theory, since it doesn’t really explain the origin of any of its “nontrivial requirements for functionality.” The author proposes that “preadaptation” might have played some role. But that adds nothing by way of explanation, since it only specifies when (before selection played a role) and where (in noncoding DNA), not how the genes in question first arose. Details about how the gene became “preadapted” for some future function is never explained. Indeed, evolutionary biologists typically use the term “de novo origination” to describe unexplained increases in genetic information; it does not refer to any known mutational process. (Darwin’s Doubt, pp. 216, 220-221.)

In other words, de novo isn’t an explanation at all. It’s more like a magic wand to be invoked when evolutionary biologists encounter some unique gene and they have no way to explain its origin via duplication from a similar pre-existing gene. (As an evolutionary mechanism, gene duplication has its own issues.)Nonetheless, a recent article in Quanta Magazine points out just how many recent scientific studies have resorted to calling upon de novo origin of genes:

For most of the last 40 years, scientists thought that this was the primary way new genes were born — they simply arose from copies of existing genes. The old version went on doing its job, and the new copy became free to evolve novel functions.Certain genes, however, seem to defy that origin story. They have no known relatives, and they bear no resemblance to any other gene. They’re the molecular equivalent of a mysterious beast discovered in the depths of a remote rainforest, a biological enigma seemingly unrelated to anything else on earth.

The mystery of where these orphan genes came from has puzzled scientists for decades. But in the past few years, a once-heretical explanation has quickly gained momentum — that many of these orphans arose out of so-called junk DNA, or non-coding DNA, the mysterious stretches of DNA between genes. “Genetic function somehow springs into existence,” said David Begun, a biologist at the University of California, Davis.

If the idea that “Genetic function somehow springs into existence” doesn’t sound compelling to you, join the club. But that’s about as much detail as you’re likely to get from proponents of de novo gene origination. One proponent of this idea in the article is even quoted saying: “It’s hard to see how to get a new protein out of random sequence when you expect random sequences to cause so much trouble.” Unfortunately for evolutionists, this problem seems to be common among animals, as the Quanta article continues:

This metamorphosis was once considered to be impossible, but a growing number of examples in organisms ranging from yeast and flies to mice and humans has convinced most of the field that these de novo genes exist. Some scientists say they may even be common. Just last month, research presented at the Society for Molecular Biology and Evolution in Vienna identified 600 potentially new human genes. “The existence of de novo genes was supposed to be a rare thing,” said Mar Alb�, an evolutionary biologist at the Hospital del Mar Research Institute in Barcelona, who presented the research. “But people have started seeing it more and more.”

Whenever you see “de novo” origin of a gene invoked, you know that evolutionary biologists lack any explanation for how that gene arose. Scientists haven’t had much time yet to analyze the cephalopod genome, but given early reports of many unique genes, it will be interesting to learn to what extent they are forced to invoke these mysterious processes — what amounts to evolution ex nihilo — to explain how this “alien” genome arose.

Why Bother Searching for ET?

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bigufoIt’s a disturbing question, and one that I seem to get more frequently than before.

“Why are you looking for evidence of extraterrestrials? What’s the point?”

While I have always thought that the motivation for looking for E.T. was both self-evident and patently worthy, it’s possible that I’m a victim of my own job description. Others don’t inevitably agree. Some will opine that there are better ways to spend the money.

“With all the problems we’re facing here on Earth — climate change, environmental degradation, war, poverty and more — why are we wasting funds looking for space aliens?”

That’s the same argument that’s often lobbed at NASA’s space programs, and at basic research in general. The thrust is that if your work isn’t obviously helping to better my lot (or maybe the lot of a lot of others), then you’re just friction in the system.

My knee-jerk rejoinder to this all-too-easy humanism is to note that the amount of money involved is tiny. The total funding of SETI (the Search for Extraterrestrial Intelligence) in the U.S. is 0.0003 percent of the tax monies spent on health and human services. And it’s not even tax money. The SETI Institute’s hunt for signals is funded by donations.

But while pointing out the realities of funding is certainly legitimate, I’ve recently promised myself to avoid doing so. It gives up too easily, and sounds like a confession: “Yes, you’re right. It’s a waste, but a very small waste.”

Well, it’s not a waste. The hunt for other sentience in the cosmos is done for reasons that could be extremely important and that, in any case, gratify the finest aspects of our spirit.

Consider the practical consequences of discovering company among the stars. These benefits are, admittedly, uncertain and hard to predict. They depend on whether we could ever decode signals from intelligence that is not only many light-years distant, but enormously ahead of us in technical ability. We’re not going to hear from beings that are at our level — they won’t have the equipment necessary to transmit a signal that today’s SETI experiments could pick up. So if a radio disturbance from ET someday floods our antennas, you can be sure that whatever’s behind the microphone would judge our own knowledge of science to be merely quaint.

Consequently, if we can make heads and tails of their signal, we could become privy to knowledge that would otherwise remain unknown until developed by our descendants centuries or more in the future. While this manna from the skies could be profoundly disruptive, you can’t argue that ignorance is blissfully preferable. It’s not.

But what if — as is thoroughly possible — we’re unable to understand ET’s broadcast? What if we just know they’re there? In the months following a detection, intense study of the signal source would garner a handful of astronomical facts — the distance to the senders, a few planetary parameters such as the length of day and the likely mean temperature, and possibly some information about the atmosphere. All of which would be interesting, and even mildly informative (did ET evolve on a world somewhat like our own?) But it would leave us guessing about the inhabitants based on the habitat. And the meaning of the message might eternally elude us.

However, even without that prize, the contest is more than worthwhile. Exploration is an oft-lauded human activity, and one that resonates in the same way that music and good stories do. It’s hard-wired into our species (and into many others), no doubt because it has survival value. Exploration occasionally rewards those who accept its risks, usually with new resources.

There’s little need to expound on the romantic lure of exploration, for few would dispute it. But there’s a special appeal in a search for other-world intelligence. We have a deep fascination for this because, after all, Darwinian mechanisms ensure that all life has a paramount interest in its own species. For us, other thinking beings are subconsciously regarded as potential equals, and interest us as competitors or mates. Of course, real aliens would be neither, but their sentience makes them compelling in a way that extraterrestrial bacteria are not.

Our curiosity is broader than merely the innate interest in cosmic doppelgangers, however. We want to know if intelligent life is some sort of wildly improbable accident. Are we the only members of the Galaxy that can actually understand what a galaxy is? Could Homo sapiens really be the pinnacle of Creation — the cleverest critters in the cosmos? If we learn the answer is “no,” that would affect our philosophies forever.

In the past I was seldom asked why we hunt for extraterrestrial company, only how. Perhaps the realities of today’s world have narrowed our vision to the near-to-hand. SETI is too speculative. And sure, concern for the immediate and the demonstrably practical is helpful in the short-term. But if we only look nearby, we can’t see where we’re going.

Frank Borman remarked that “exploration is really the essence of the human spirit.” Borman’s an astronaut, so he was tipping his hat to his own career. And so am I when I say that SETI is done out of curiosity, and is both tremendously exciting and undoubtedly worthwhile. It might alter the trajectory of our civilization. But more than that, a search for others feeds the best in our nature.

UFO News , Alien Life , Paranormal , Outer Space , Seti , Science News

Source: http://www.huffingtonpost.com