"I put the ways of childhood behind me" — my remembrance of Dan Dennett

For five years through 2018, our humanist community, the Humanist Hub*, met every Sunday afternoon at our suite in Harvard Square for fellowship, music, and a speaker. Our advisory board included luminaries of humanism such as Rebecca Goldstein, Steven Pinker, and Dan Dennett. These friends of the organization regularly spoke at Humanist Hub events. One of the most memorable, for me, was Dan Dennett's talk in November 2017, "The Science of the Soul (and where to go from here)."

I was lucky enough to be asked to introduce Dan, and shared thoughts about what his work had meant to me. I've included my lightly edited script below. The video on Facebook includes more jokes (and laughs) and shows a typical Sunday program at the Hub. The program starts at 13:30, with music at 20:30, my remarks starting at 27:30, and Dan's talk starting at 37:20.

Science, intuition and the "strange inversion of reasoning"

A few days ago I wrote about scientific thinking as an antidote to intuition. Not just an alternative to it, but something like the opposite of intuition. The intentional, energy-consuming move to a systematic deliberative mode of thought is utterly different from the easy and instantaneous nature of intuition.

Some of our intuitions are clearly built-in. Many of the famous failings of our intuitive System 1, described by Daniel Kahneman in Thinking, Fast and Slow, seem to be hard-wired. Some are perhaps the unavoidable result of trade-offs that buy speed and decisiveness at the expense of accuracy and completeness. Others might be adaptive despite being occasionally delusional: I'm thinking here of optimism bias. Some days we just need some good old optimism bias!

But some of our most famous intuitions are more complex and a bit harder to attribute to brain wiring or adaptive tricks. These are intuitions that seem to affect how we see the whole world, all of existence, all day. I think it's intuition (and nothing else) that makes us feel that something complex, that shows design, must have come from a designer. That a universe has to have a beginning, and therefore a "beginner." That a mind like ours must somehow come from a bigger mind somewhere else. That seemingly uncaused events must have had a cause. Which are all probably related to a sense that the universe is haunted.

I'm not sure that these intuitions are all universally human—some are likely to be deeply cultural. But the point is that well beyond our intution that the sun moves through the sky or that the earth can't be a spinning ball, there are intuitions about the very fabric of existence.

Design without a designer: explaining and answering some questions

I've been writing and thinking about design in biology since I started Quintessence of Dust. I want to write and think about it a lot more, so in my last post I introduced my view of the concept and pointed ahead to this post, which consists of edited excerpts from some conversations at a discussion forum at the Peaceful Science site. You will find links to those conversations in the previous post. I have removed people's names and lightly edited for clarity. Other people’s words are indented; the rest are mine.

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I would like to understand better how you think about it because it seems quite different from the way I normally think about it. I would really like learn more about how you see it and expand my understanding of "design".

This is a potentially big interesting deep conversation that is worthy of a dedicated thread with some clear goals. Someday I’ll propose that, since I believe that we can improve the quality and tone of conversations about biological design by getting at least some unbelievers to agree that design in biology is an interesting and worthy question that need not and should not have inherent religious overtones.

I guess my first question for you as you compare your conception of 'design' to mine is this: do you think design is something that is done (by a designer) or do you think it is something that exists and can be detected by humans? Obviously both can be true, but as long as a person believes that 'design' necessitates a 'designer', then they won’t see design the way I do. Because my view is that design exists whether or not it is linked to a designer. To me, it is axiomatic that a mindless process can generate design, not only because we have seen it happen but because there is no good argument to the contrary. It is instructive, IMO, that the "argument" offered to the contrary is something like "all of our examples of design can be traced back to a mind." This is not even an argument.

But what do we mean by 'design'? Here I think we can look at some of the definitions and conceptions offered by the ID movement. I think Behe’s "purposeful arrangement of parts" is a nice start, because it captures something that we all detect when we consider (for example) a molecular machine. Was a bacterial flagellum designed by a designer? I don’t know. Does a bacterial flagellum evince design? To me, the answer is obviously yes.

Design without a designer: the "British tendency" and introduction

One of the most interesting books I've read in the last few years was The Gene's-Eye View of Evolution by J. Arvid Ågren. The author explains the gene's-eye view both scientifically and historically, and I hope to write about the book sometime soon. But for now there's one point he makes that I found fascinating. Citing Kim Sterelny (an Australian philosopher of science who has written on personalities in evolutionary biology, esp. Gould vs. Dawkins), he identifies two major emphases (Sterelny calls them "tendencies") in evolutionary biology: the American interest in diversity and the British interest in design. These are pretty crude distinctions, at least because examplars of the "British tendency" include Americans like Dan Dennett. But the point is that one of two major streams of thought in evolutionary science is the challenge Paley made famous and that inspired Darwin—the one that inspired The Blind Watchmaker and its author. It's the challenge of explaining design in the biological world, and the most notable characters in that story are Brits from three very different generations.

Schematic representations of the type IV filament superfamily of nanomachines, from Figure 1 of Denise et al. 2019

I'm not British (I'm just a wannabe) but I'm drawn to that question too. My interest is probably partly due to my time served as a Christian believer, since the Christian god is a common unworthy beneficiary of the curiosity and wonder that nature inspires in humans. I have always objected to the whole construction: we see cool and extraordinary stuff in nature, we don't seem to have an explanation, so we turn to a god as an "answer." Nothing about those stories appealed to me, not when I was a committed believer and not now that I am an emancipated apostate. One problem, that I've mentioned before, is that I am apparently of the British tendency: I see the design, and I want to explain it. Design is the question, and not the answer to any interesting question. Design is what I see. I don't need a religious apologist to convince me that it exists.

Beshrew my heart but I pity the man. Final reflections on From Extraterrestrials to Animal Minds by Simon Conway Morris

I've reviewed a few books over the years here at Quintessence of Dust, but From Extraterrestrials to Animal Minds: Six Myths of Evolution by Simon Conway Morris was the first book I blogged through that I was genuinely excited about reading. I bought it sight unseen, new and in hardcover, from a publisher of dubious reputation, because I was beguiled by the author and the title and what I mistakenly believed that title to mean. I have already written that I regretted paying money for the book once I read the first couple of chapters and realized I'd been had. From Extraterrestrials to Animal Minds isn't about myths, nor is it about interesting controversies, and its ideas/claims are mostly recycled from previous works by the author. In retrospect, the book didn't merit the attention I gave it, and it doesn't merit yours.

David Strathairn and Sophie Marceau as Theseus and Hippolyta in A Midsummer Night's Dream (1999)

But that doesn't mean I regret the exercise as a whole. Writing my way through the book helped me clarify some of my own thoughts and ideas. So this post is as much about me and my ideas as it is about the book.

If it's not natural selection, then it must be...

The folks at the Discovery Institute (DI) are engaged in an extensive attempt to rebut my friend Dennis Venema's critiques of Stephen Meyer's surprisingly lame ID manifesto, Signature in the Cell. There are several aspects of this conversation that I hope to address in the coming days and weeks, but one jumped out at me today: the consistent confusion about natural selection in depictions of evolutionary theory by design advocates.

Consider this excerpt from a recent blog post by a writer at the Discovery Institute:

...we need a brief primer in fundamental evolutionary theory. Natural selection preserves randomly arising variations only if those variations cause functional differences affecting reproductive output.

A few sentences later, the same claim is repeated:

Indeed, given that natural selection favors only functionally advantageous variations, ...

Those claims were first made in a piece written by unnamed DI "fellows" mocking the work and conclusions of Joe Thornton, an evolutionary biologist at the University of Oregon and the University of Chicago. And the claims are badly misleading.

Design and falsifiability

Last month I had an interesting conversation with Casey Luskin of the Discovery Institute (DI), at Evolution News and Views (ENV), a DI blog/site that recently opened some articles to comments. The topic of the original post was common ancestry in humans and other primates, but Casey and I discussed various aspects of design thought.

One subject that came up was the falsifiability of design. I maintain that design arguments, whenever they also postulate the existence of an omnipotent deity (or any super-powerful being, for that matter), are inherently unfalsifiable. And I want some feedback on my argument.

Alu need to know about parasitic DNA: telling the whole story about Alu elements and "design"

So, Alu elements are mobile DNA modules that can exert diverse influences on genomes and the organisms harboring them. They can affect genome function in constructive ways, by altering gene expression or supporting chromosome structure. And they can be damaging, even deadly. There are more than a million of them in the human genome, and we don't know what each one does. But, as I explained in the first post in this series, we do know that they can play both helpful and harmful roles, in the same way that other kinds of parasites can be good, bad, or indifferent.

Alu elements and other genome-wide repeats are a big problem for intelligent design (ID) theorists of some stripes. Any ID proponent who claims that genomes are carefully-designed, well-optimized systems must deal with the reality of the enormous numbers of mobile elements in (for example) the human genome. Now, I can think of various ways such an ID theorist might discuss Alu elements. She could propose that all of their characteristics (including their mobility) are part of their design, such that they can bring new design features quickly into being; she could propose that their mobility is a "bug" rather than a "feature," and perhaps speculate on how things went wrong; she could postulate that the damage caused by their expression and their mobility is being misattributed to the genome when it is instead caused by some other external process. (Or she could say, "We're still working on that one.")

Exploring the protein universe: a response to Doug Axe

One of the goals of the intelligent design (ID) movement is to show that evolution cannot be random and/or unguided, and one way to demonstrate this is to show that an evolutionary transition is impossibly unlikely without guidance or intervention. Michael Behe has attempted to do this, without success. And Doug Axe, the director of Biologic Institute, is working on a similar problem. Axe's work (most recently with a colleague, Ann Gauger) aims (in part, at least) to show that evolutionary transitions at the level of protein structure and function are so fantastically improbable that they could not have occurred "randomly."

Recently, Axe has been writing on this issue. First, he and Gauger just published some experimental results in the ID journal BIO-Complexity. Second, Axe wrote a blog post at the Biologic site in which he defends his approach against critics like Art Hunt and me. Here are some comments on both.

Introns. Let's think about this, people. Part IV.

So why is it that I and many other biologists hypothesize that introns are mostly non-functional?

(I'll assume that you've read the previous posts, and that you understand what it is that I mean when I challenge claims that introns are functional elements in an information-rich genome. And to avoid confusion, I'll speak only for myself, although I surmise that a tiny minority of biologists would agree with creationist characterizations of the human genome.)

Here are the basic data that lead me to conclude that intron sequences are mostly dispensable for biological function. I've provided links to key references, and we can go into more detail in further posts or in the comments.

Bread and circus: Signature in the Cell at Biola (Part III)

Here I'm continuing my discussion of the Signature in the Cell book-signing event at Biola University on 14 May. You'll want to read Parts I and II before reading on.

My second question to Steve Meyer was the one question I most wanted to ask him, both out of personal curiosity and because I thought the answer would help demystify many of his claims. The exchange that resulted was memorable – on that, everyone seems to agree. But the nature of my comments has been profoundly misrepresented by Meyer's hired guns. I hope that this will be crystal clear when I'm done here.

Signature in the Cell: Chapter 8

It's been a month and a half since my last post in this series, and recently a friend asked me why I stopped. I can think of two reasons: first, I spent the month of March teaching a graduate course for the first time; second, I'm worried about how this is going to go. I'm worried because I can see that the book is poor scholarship – Meyer is either underinformed or overcommitted to his cause – and I can see that my critique will be considered within a religious milieu that hinders straightforward criticism and analysis. Ergo, I think this might not be very pretty. It would be a lot more fun to blog about any of 15 different papers from the last two issues of Nature.

But we need to finish, partly because I'll be on a panel of critics at an event with Stephen Meyer himself in Los Angeles next month. (Not just critics: "a powerful group of credentialed critics." More later.)

Chapter 8 is called "Chance Elimination and Pattern Recognition." It deals first with the notion of chance and then with subjects that are at the very heart of design thought – the dual consideration of improbable events and the genesis of phenomena that exhibit "patterns." The chapter is pretty good, but seems to contain seeds of significant future confusion.

Introns and design

Mike Gene has posted an interesting series on introns that's worthy of a few comments. His thesis is that "introns facilitated the evolution of multicellular life."

A. The idea is interesting and rational but not novel. Research on introns and evolution is active and lively, and one prominent scientist in the field, Eugene Koonin, has proposed that introns drove many aspects of the evolution of eukaryotes (i.e., non-bacteria).

Signature in the Cell: Chapter 7

The chapter is called "Of Clues to Causes" and it's about scientific explanation. That's an interesting and important topic, one that opponents of evolutionary theory rarely understand. Meyer's summary is predictably fluffy but not inaccurate. Those seeking an introduction to philosophical questions pertaining to scientific explanation should look elsewhere, since Meyer says little in the 22-page chapter. His main points:

1. There are indeed legitimately scientific means of understanding and seeking explanation for past events.
2. These approaches validate ID as a "possible scientific explanation for the origin of biological information."

I don't disagree with either assertion. But neither is particularly helpful to ID in its quest for explanatory relevance. (Well, the main quest of the ID movement is to undermine naturalism by any means necessary, but its scientific challenge is to demonstrate that it can provide useful explanation.)

Signature in the Cell: Chapter 6

The chapter is called "The Origin of Science and the Possibility of Design." It's short, unimportant and uninteresting. Its purposes, along with Chapter 7, are twofold: 1) to counter the claim that ID theory is "not science" and 2) to establish that "historical science" (that which deals with the past) is not all that different from "operations science" (as defined by Charles Thaxton and others), specifically because the theorizing of "historical science" can be considered testable.

Signature in the Cell: Chapters 4 and 5 - errors and problems

Meyer's basic idea in chapters 4 and 5 is reasonably coherent. But I find further evidence in both chapters that Meyer is careless and underinformed on the subjects he addresses. (I explained before why I think this matters. If you think I'm not being nice enough to Meyer, consider providing me with the Rules of Engagement that apply when criticizing culture warriors who are proposing world-shifting new ideas.)

Signature in the Cell: Chapters 4 and 5 - major themes

Chapter 4 is called "Signature in the Cell." It's an important chapter for two reasons. First, along with chapter 5 ("The Molecular Labyrinth") it lays out Meyer's central question by pointing to the specific features of cellular information systems in need of explanation. Second, it exemplifies an aspect of ID thought that I want to highlight. I'll discuss these two themes here, then add some further critiques in a second post.

Signature in the Cell: Chapter 2

The chapter is called "The Evolution of a Mystery and Why It Matters." It's interesting and engaging, and I enjoyed reading it. The "mystery" in question is first described on page 35:

...most philosophers and scientists have long thought that Darwin's theory of evolution by natural selection destroyed the design argument. Yet I also discovered that Darwin himself admitted that his theory did not explain the origin of life itself. [...] His theory assumed rather than explained the origin of the first living thing. Since this limitation of Darwin's theory was widely recognized, it raised a question: Why were nineteenth- and twentieth-century biologists and philosophers so sure that Darwin had undermined the design argument from biology?

Deep homology and design: why Notch?

The Notch signaling pathway is a golden oldie of genetics in two ways. First, it's a system that was first described at the dawn of modern genetics – named by its founder, Thomas Hunt Morgan – and used to establish some of the most basic principles of "the physical basis of heredity," as Morgan put it. (His book by that title is a founding document of modern genetics, describing in 1919 what we now call chromosomes without any knowledge of their chemical makeup.) Second, it's a system now known to be as ancient as animals themselves.

Why Notch? The name refers to the appearance of some of the first mutant fruit flies described by Morgan and his colleagues in their famous work in the early 20th century. They found flies with notched wings, and found that the trait was dominant.

Figure 1 from T.H. Morgan, "The Theory of the Gene." American Naturalist 51:513-544, 1917.

So aside from its importance in evolution and development, Notch is of historical interest to genetics. Now, Morgan was interested in Notch (the gene name is capitalized because the original trait is dominant, in case you're wondering) because of its mode of inheritance, not specifically because of its biological effects. (I mean, who cares about flies with notched wings?)

But twenty years later, things got more interesting when a different mutation in Notch was found to cause a weird (and lethal) overgrowth of the nervous system. Interesting... then, as geneticists began to probe the genetics of animal development 50 years after Morgan's initial discoveries, using the fruit fly as a model, Notch started turning up again and again. Problems in Notch signaling led to developmental problems all over the place: brain, eyes, gut, wings, bristles.

By the beginning of the 1990's, geneticists had figured out why its activity is so central to proper development: Notch controls a crucial type of cell-to-cell interaction that leads to a change in cell fate. And they had found Notch signaling in animals of every kind, including in humans, mediating the same kinds of inductive developmental interactions. It's not as complicated as it might sound – in such an interaction, two cells interact physically (they have to touch) and after the interaction one or both of the cells changes its developmental fate, choosing to become, say, a nerve cell or a skin cell. That weird brain overgrowth in the flies with no Notch activity results from a failure of cells to communicate in this way, such that all the cells on the outside of the fly's head become brain cells. (Flies, like most animals, prefer to have some skin over their brains, but in these mutants there's very little skin and lots of extra brain. Ick. See Figure 1 of this recent paper in BMC Biology for pictures; the green stain indicates nerve cells and the second animal down has the nasty trait.)

The point is that Notch signaling involves direct cell contact, and typically leads to cells making decisions about what to do when they grow up. So how does it work? Well, we know an awful lot about this particular system, and there are myriad details of mechanism and control that I'm going to skip. The very basic outline is as follows. Some cells make the Notch protein, which is a receptor. Other cells make the Delta protein, which is the signal that activates the receptor. (One useful analogy is that of locks and keys: Notch is the lock, Delta is the key.) Both proteins are displayed on the cell surface. When the two cells come into contact, the Delta protein on one cell activates the Notch protein on the other. When Notch becomes activated, it gets chopped into at least two pieces. One piece leaves the surface of the cell and travels inward to the nucleus of the cell. There, in collaboration with other proteins, it causes changes in gene expression, meaning that some genes are turned on or up and others are turned off or down.

This mode of signaling is unique and extraordinary. What we have is a signaling system that takes cell-to-cell contact and converts it directly into changes in gene expression.

Now, let's think carefully about this. We have a system of receptors and activators, in the form of Notch proteins (there are at least four in humans) and Delta proteins (there are several in humans, in a few different protein families), which serve a critical and unique purpose in cell-to-cell signaling. The function is conserved in all known animals, and that's not surprising – having cells send messages to their immediate neighbors, directing them to adopt particular fates, is key to constructing tissues and organs. I hope you'll agree that we should expect to see these inductive mechanisms in the development of complex organisms. More to the point, one should expect this regardless of one's stance on questions of "intelligent design."

Here's what is surprising. The same Notch proteins are used for this purpose in every known animal. And here's why that's surprising: as far as we know, there's no reason to insist on those particular proteins playing those particular roles. It's easy to envision – and then design and create – a set of locks and keys that bear no resemblance to Notch or Delta but that can accomplish these somewhat basic purposes just as well. There's no need for such a specific solution to a basic challenge. Why does every animal use Notch? Recall the previous post in this series and how we approached this question of common design. Here, again, are our options.

1. These inductive signaling events could only be accomplished by Notch. There is a design constraint, currently unknown, which forces that choice. It may seem that the system could have been effectively constructed using a different lock-and-key combination, but in fact it could not function (or function well) any other way.
2. These inductive signaling events could be mediated in various ways, but the choice of Notch has been forced by common ancestry. The earliest animals settled on this choice, and their descendants have used it ever since.
3. These inductive signaling events could be mediated in various ways, but an intelligent designer has repeatedly chosen Notch for reasons known only to her/him/it.

Option #1 is, in my view, unreasonable. The system is not complicated in its basic design. There are no clear constraints on the choice of lock and key. A designer who is crafting an organism from the ground up need not select that particular lock/key combination, and someone who intends to argue otherwise needs to demonstrate how that particular combination is superior.

Option #3 is, I think, perfectly reasonable. The only problem is that one must know quite a lot about the designer to begin to surmise her/his/its goals and proclivities. Without that knowledge, it is no more reasonable to assume a preference than it is to assume a constraint.

The point is not that we can ever rule out preferences or other characteristics of a creator or designer. The point is that we can rarely make explanatory use of them. Consider that while we may assert that the Creator/Intelligent Designer prefers that pine trees have needles, we would not advance that as a useful explanation for why pine trees have needles. Specifically, we would never advance that as an alternative explanation in place of one that notes that today's pine trees have the same needles that last century's pine trees had, by virtue of biological ancestry.

Notch signaling represents one of the classic examples of deep homology. It seems to me that design theorists need to deal with deep homology before they can ever be taken seriously as scientific thinkers. Deep homology is crying out for explanation, and those who believe that the biosphere cries "design" are remiss in not offering a serious design-based explanation for the fact that every animal on the planet uses the same lock-and-key mechanism to achieve basic cell-to-cell inductive communication.

Next, we'll look at a recent and very interesting example of new findings that illustrate the striking conservation of Notch-mediated developmental events – an example of deep homology that could arise from the very root of animal ancestry.

Deep homology and design: common design and its implications

Consider these not-so-random samples from the animal world: a cockroach, a zebrafish, a mouse. What do these creatures have in common?

Left to right: American cockroach (Periplaneta americana), zebrafish (Danio rerio), house mouse (Mus musculus). Cockroach image from Wikimedia Commons, zebrafish and mouse from Wellcome Images.

Well, they're all animals and that means they're all eukaryotes, for example. They all have DNA-based genomes. They all like water to some extent. They all have muscles that cause them to move. And so on.

But let's think of them in a different way. Let's think of them as things that exhibit design. (Not Design. Just design.) We see similarities like the ones we just listed, and we see some dramatic differences. Insect, exoskeleton, open circulatory system. Fish, gills, egg-laying. Mammal, milk, hair, live birth, temperature control. We can see elements of common design (limbs and joints, eyes, nerves) and elements of specialized design (lungs, fins, antennae).

Now let's forget everything we know about common descent and adopt an Intelligent Design perspective. This isn't hard to do: just think of each animal as a machine that was designed to be the way it is. The machines have some common design elements and some specialized design elements. Now this is important: let's assume that each machine was designed separately, such that design decisions were made on a case-by-case basis (for each type of machine, not for each individual machine). In other words, let's think of the cockroach as designed from the ground up to be a cockroach, and the fish and the mouse likewise. Simple, right? I think so.

Now, let's look under the hood of each machine and ask detailed questions about how it's built, again with the assumption that it was designed. Not just its overall structure, but also the procedures used for its assembly. Let's look, in other words, at its molecular machinery – machinery for signaling between cells and tissues, machinery for signaling within individual cells, machinery for directing gene function during development and normal function. And let's focus specifically on the signaling systems in these creatures and in their developmental stages. What would we expect to see? Well, let's consider some basic scenarios.

1. Maybe the signaling systems will be roughly the same – or even largely the same – in all three animals. This would imply that such systems are hard to assemble and perhaps even harder to tune and maintain, and therefore we would conclude that there are very few ways to make a working system. The only other explanation would refer to preferences on the part of the designer, who was unconstrained by design limitations but nevertheless insisted on doing things a certain way.

2. Maybe the signaling systems will differ between the three animals, to such an extent that it is clear that the choice of a system is somewhat arbitrary, arbitrary in the sense that the choice of a particular system is largely independent of the context or the function that is specified. The implication is that there are plenty of ways in which cells and molecules can communicate, and no strong constraints on the designer's choices.

Now of course we may find examples of both scenarios in our analysis. Perhaps some signaling systems will appear to be highly constrained while others will be largely different among the three species. The point, though, is this: when examining machines that were separately designed, common design implies either design constraint or designer preference. Divergent design implies a lack of design constraint. There are no further options: either the designer was constrained, or she wasn't; if unconstrained, she could nevertheless choose a favorite scheme and leave the impression that she was somehow constrained.

Designer constraint could arise in various ways. It could be that a particular signaling system is uniquely suited to a particular purpose. It could be that a particular signaling system is highly robust to damage or other challenges. It could be that there are only a handful of different possibilities due to limitations in the raw materials. One variation of that last possibility would look a lot like how evolution is known to work: the designer tweaks the system a little at a time, working with the materials supplied by each generation and therefore constrained by common descent.

Design proponents can be stunningly cavalier about all this. "Common elements in animal biology? Well of course! Common design!" But wait: common design implies either design constraint (that was the best way to do it – or the only way to do it) or designer preference (she just happens to like it that way), and those are dramatically different from an explanatory standpoint.

It turns out that signaling systems in animal development are so universally conserved that they require an extraordinary explanation. The commonality of the elements is so striking that it took most biologists by surprise when it first became evident, and remains one of the most remarkable facts of developmental biology today. We'll look at some recent advances in this area of evo-devo in posts to come.

But one last thing: I'd like to try a thought experiment to illustrate how we might approach questions of signaling in animal cells and embryos. Consider a group of 50 people who have agreed to help with your experiment. You divide them into pairs and tell each pair to send one person out of the room. Then you tell the remaining people to greet their partners upon their return, using a single word of their choosing that is certain to convey the greeting. You observe that all of the people employ either "hello" or "hi" for this purpose.

Question: would you conclude that "hello" and "hi" are uniquely suited for the task, and that no other word could possibly have worked? I hope you would seek another explanation and perhaps consider trying the experiment in, say, Shanghai or Guadalajara. You would conclude, I wager, that the word itself is of little explanatory value. In other words, the choice of a word was constrained, but not by anything specific to the word itself. In Shanghai, it's "ni hao." Maybe somewhere it's "duuuuuuude." And in a matter of minutes, you could change it to "ahoy" or "blorp" or anything you want.

And if you really wanted to probe the notion of constraint in human conversation, you would ask your 25 pairs of subjects to come up with an identifying word or phrase that they could call out to find each other in the dark. You would find, of course, that the choice of that word or phrase would be almost completely unconstrained.

What does all this have to do with signaling systems and design? That's for next time. Till then, blorp.