At least, I’m pretty sure.

That’s Homo longi, or Dragon Man, a recently rediscovered fossil from China. It has a curious history.

Almost 90 years ago, Japanese soldiers occupying northern China forced a Chinese man to help build a bridge across the Songhua River in Harbin. While his supervisors weren’t looking, he found a treasure: a remarkably complete human skull buried in the riverbank. He wrapped up the heavy cranium and hid it in a well to prevent his Japanese supervisors from finding it. Today, the skull is finally coming out of hiding, and it has a new name: Dragon Man, the newest member of the human family, who lived more than 146,000 years ago.

Here, take a tour of the skull with Chris Stringer:

That is a big head-bone! The most provocative idea about it is that it might be one of the mysterious Denisovans, known only from DNA and fragmentary teeth.

I’ve been so deeply steeped in spider lore lately, though, that my perspective has shifted to finding it hard to believe in species anymore anyway. It’s cool to see that humans were also a diverse clade with subtle variants 150,000 years ago, almost as messy and complicated as, say, the Tetragnatha.

This morning I have to go into the lab and do upkeep on the spider colony and then I come back, put a big diet Coke by my side, and settle down to this schedule.

It’s time for the grindy part of the meeting! See that “contributed talks” bit? That’s 5 hours of 15 minute talks, one after the other, with occasional breaks during which, in a normal meeting, you’d mill around and talk to other people, but here in Virtual World I’ll just get up and stretch and walk in circles in my little office, I guess. They have concurrent tracks, so I can’t possibly see all the talks and have to miss half of them, so I think I’ll have to focus on the evo devo stuff, and then behavior, and then ecology & diversity. It’ll be a grueling session, but I’m looking forward to it.

Then we do it all again tomorrow.

Then again on Wednesday morning.

There are conveniences about online meetings, but I’m still hoping to go to the in-person meeting next year at UC Davis.

For the past month or so, my inbox has been inundated with letters insisting that they have proof of the lab leak hypothesis for the origin of SARS-CoV-2. Their insistent missives are full of jargon, like arginine codons and furin cleavage sites, and insistence that the particular sequence found in the virus could not possibly have arisen naturally. I am not an expert in viral genomics by any means, so my usually reply is a shrug that I don’t know the details, but I find their claim that the viral sequence could not have appeared by natural causes to be naive and unlikely, and that their probability argument is not a clincher. I’ve usually refrained from pointing out that they sound exactly like a few generations of creationists I’ve had to put up with.

A lot of that jargon and argument can be traced back to an article by Nicholas Wade in which he made those very same claims. I tend to veer away from anything by Wade — his embarrassingly bad book that advocated for “race realism” convinced me he’s not a trustworthy source — so I didn’t dig deeply into it. He seems to have persuaded some people, including David Baltimore(!), who has since retracted his endorsement of Wade’s “smoking gun”.

A science writer I trust far more, Thomas Levenson, explains what’s wrong with Wade’s claim.

Wade asserted that a particular arrangement of a specific sequence in the viral genome, called a codon, was unlikely to have gotten there naturally. There are actually six different codons for arginine, and the one found in a particular region of the SARS-CoV-2 genome called the furin cleavage site does occur less frequently in viruses than it does in the human genome. An even more telling detail to Wade is that this uncommon arginine codon shows up twice in that small segment of the virus’s genome. For that to occur naturally, Wade wrote, “a chain of events has to happen, each of which is quite unlikely.”

That’s what Baltimore assented to. But scientists say Wade misdescribed critical links in his chain. Scripps Research virologist Kristian Andersen led an early inquiry into the possible role of a lab escape in the origin of the virus, which concluded that it “is not a laboratory construct,” a finding that Wade termed “poor science” in his article. After Baltimore’s quote became public, Andersen re-entered the argument, and became one of a number of researchers to challenge many of the details Wade relied on. Andersen told Nature that Wade’s claim that steps in the emergence of the virus were too improbable to have occurred is not true. Rather, the pandemic virus uses that codon about 3 percent of the time that its genome calls for arginine—not common, but not impossibly scarce either—and, importantly, that other coronaviruses make use of it too, at similar or greater frequency.

Columbia University virologist Vincent Racaniello says the unusual pairing of a particular codon that Wade saw as decisive actually points away from laboratory manipulation. “We have some idea why this codon is rare in RNA viruses,” Racaniello says. Selection pressures have been identified that would discourage its use in viral genomes. But, he says, “We don’t know why it’s not zero. The fact that it is conserved in many viruses means that it’s beneficial in some way we don’t understand.” This is the kind of mystery that evolution throws at researchers all the time. Racaniello adds that if a lab researcher was trying to modify a virus to measure its effect, the researcher wouldn’t use the codon pairing identified by Wade because its effect would be too unpredictable.

I’d had an uncomfortable feeling with any argument that claims a low probability makes something impossible, because improbable things happen all the time. But 3%! That’s not low, especially not when you’ve got a virus with a population of trillions.

The SARS-COV-2 virus is certainly benefiting from the power of natural selection. It’s spreading rapidly through a vulnerable population, that is us, and we’ve been half-assing our response, which simultaneously allows it to proliferate in large numbers and yet also favors variants that can overcome what barriers we do put up. What that means is that new strains will continue to pop up and take a run at our immune systems, and some of them will do better than the original strain. On an abstract, very academic level, it’s kind of cool. On a human level, it’s a disaster that threatens to get worse.

Right now, we get to deal with the Delta variant. It seems to have arisen in the giant petri dish we call India, but now it’s everywhere.

The B.1.617.2 coronavirus variant originally discovered in India last December has now become one the most — if not the most — worrisome strain of the coronavirus circulating globally. Recent research suggests it may the most transmissible variant yet and has fueled numerous waves of the pandemic around the world. B.1.617.2 has already spread to at least 62 countries, including the U.S., and undoubtedly contributed to the massive wave of cases that has inundated India in recent months. It also appears to have become the dominant strain infecting unvaccinated people in the U.K., and may be more likely to infect people who are only partially vaccinated than other strains. Below is what we know about B.1.617.2 — also known as the Delta variant.

How is B.1.617.2 different from other variants, and why may it be more dangerous?
The Delta variant has multiple mutations that appear to give it an advantage over other strains. The most important apparent advantage is that the mutations may make the strain more transmissible, which would also make it the most dangerous variant yet. One study indicated B.1.617.2 may be up to 50 percent more transmissible than the B.1.1.7 (U.K./Alpha) variant. Professor Neil Ferguson, a leading epidemiologist at Imperial College London and one of the chief pandemic advisers to the U.K. government, said on June 4 that the “best estimate at the moment” is that Delta is 60 percent more transmissible than Alpha, which is itself more transmissible than the original strain of the coronavirus that emerged in China in late 2019 — and that is why scientists believe it became a dominant variant globally.

Ah, yes, the terrible beauty of evolution. It works a little too well sometimes, and it’s the fast-breeding, large population size species that benefit most. I suppose a disease that’s going to hit anti-vaxxers hardest could be seen as a brutal Darwinian benefit, except remember that all those unvaccinated people are an easy reservoir for further experimentation by the virus.

A variant with higher transmissibility is a huge danger to people without immunity either from vaccination or prior infection, even if the variant is no more deadly than previous versions of the virus. Residents of countries like Taiwan or Vietnam that had almost completely kept out the pandemic, and countries like India and Nepal that had fared relatively well until recently, have fairly little immunity, and are largely unvaccinated. A more transmissible variant can burn through such an immunologically naïve population very fast.

Increased transmissibility is an exponential threat. If a virus that could previously infect three people on average can now infect four, it looks like a small increase. Yet if you start with just two infected people in both scenarios, just 10 iterations later, the former will have caused about 40,000 cases while the latter will be more than 524,000, a nearly 13-fold difference.

This is going to have further human costs. The Delta variant has tragically cropped up in Finland now. This is a global pandemic — you may think you’ve got it under control in your neighborhood, you may be getting cocky and think it’s time to party, but it’s not over yet, and the disease kills human beings.

THE OUTBREAK of the Indian coronavirus variant in Kanta-Häme Central Hospital in Hämeenlinna, Southern Finland, has resulted in nearly 100 infections and, directly or indirectly, 17 deaths.

Sally Leskinen, the chief medical officer at Kanta-Häme Hospital District, revealed yesterday in a news conference that the chain of infection started early last month with a patient who had contracted the transmissible variant from a close contact who had travelled outside Europe.

Further infections were detected in two hospital wards on 12 May, prompting the hospital to begin widespread screening of patients and staff.

“The virus had spread from the first patient through asymptomatic staff members,” said Leskinen.

A total of 57 patients and 42 staff members have been infected in the cluster, with 17 of the patients dying after being infected. Of the infected patients, 41 had received the first dose and two both doses of a coronavirus vaccine. While the infection is estimated to had a direct link to three-quarters of the deaths, it was not ruled as the primary cause of death for the remaining one-quarter due to a serious underlying illness.

One of the deceased patients had been vaccinated twice and 11 once, whereas five of them had yet to receive the first vaccine dose. The ages of the deceased ranged from 60 to 100, with the mean being 80.

Remember, people are fragile. We’ve got a disease that exploits that fragility and is expanding its power. Don’t think it’s done yet.

On Saturday, I wrote this bit about whether animals feel pain, and I said then I’d follow up that day or the next. I didn’t! I’ve been doped up on painkillers and my brain is all soft around the edges. I finally decided to give up on them this morning when I woke up, had breakfast, and then fell asleep for a couple of hours. Enough already. Now I have to recover from some potent drugs as well as my back pain.

Anyway, where were we? Oh, right, we had taken down William Lane Craig’s argument that humans (and maybe some other primates) are the only creatures on the planet that actually feel pain, that other animals are mere meat robots who act out a superficial script that looks like they are in pain, but really, they have no consciousness to experience the pain.

I don’t think he is making this argument to warrant or excuse animal torture, but rather he’s trying to justify human exceptionalism. See, humans have this special god-granted ability to perceive suffering and pain, which is why we have souls and animals don’t, and why we have to worry about that Final Judgment, since we can sense and appreciate the harm we do to others. At least, that’s my charitable assessment.

Curiously, in order to make this argument, Craig feels a need for some scientific backing, some recognizable neuroanatomical feature that shows humans are special. I don’t get it. He already believes in something invisible and intangible, the soul, so why not just say humans posess an invisible magical flimflam that the scientists can’t see or experiment on, neener neener, therefore humans are unique in having a conscience or ghost or pneuma that gives them the abilty to really truly deeply feel pain and suffering?

Often the physical substrate for feeling pain is determined in a backwards sort of way: we find some feature of the human brain that is only found in us, or is more pronounced in us, and we decide that, aha, that must be where this higher ability resides. Some of the common culprits are our enlarged pre-frontal cortex (PFC) or more narrowly, the anterior cingulate cortex (ACC). The ACC was a favorite of Francis Crick, for instance, who thought that not only was it the seat of awareness, but also of free will (I think free will is a non-existent phenomenon that makes no sense, but I’ll defer on discussing that to another time).

I don’t think the hypothesis is far out of line — there is evidence that lesions in this area do cause sensations of dissociation, and it is entangled in a lot of higher brain functions. But on the other hand, other animals have these structures, so how do you use this phenomenon to make humans exceptional? You can’t.

This leads me to an article in a journal called Philosophical Psychology, Against Neo-Cartesianism: Neurofunctional Resilience and Animal Pain by Halper et al.. Mixing philosophy with psychology and throwing in a lot of ethology and neuroscience sounds like a potent way to address the issue, don’t you think? Especially with a feisty abstract like this one:

ABSTRACT: Several influential philosophers and scientists have advanced a framework, often called Neo-Cartesianism (NC), according to which animal suffering is merely apparent. Drawing upon contemporary neuroscience and philosophy of mind, NeoCartesians challenge the mainstream position we shall call Evolutionary Continuity (EC), the view that humans are on a non-hierarchical continuum with other species and are thus not likely to be unique in consciously experiencing negative pain affect. We argue that some Neo-Cartesians have misconstrued the underlying science or tendentiously appropriated controversial views in the philosophy of mind. We discuss recent evidence that undermines the simple neuroanatomical structure-function correlation thesis that undergirds many Neo-Cartesian arguments, has an important bearing on the recent controversy over pain in fish, and puts the underlying epistemology framing the debate between NC and EC in a new light that strengthens the EC position.

In one corner, the Neo-Cartesians like William Lane Craig (there are also secular philosophers who like this idea).

In the other corner, the Evolutionary Continuity camp, which I would happily attach myself to, which argues for “a non-hierarchical continuum with other species and are thus not likely to be unique”. Yay Team EC!

The paper quickly dispatches part of the argument. All mammals have a prefrontal cortex, although the human PFC is relatively larger. So now you’re going to have to argue, if you think the PFC is the seat of awareness, that a quantitative difference leads to a qualitative change, and you’re also going to have the problem of a continuum of PFC sizes. Where do you draw the line?

Well, maybe it’s the anterior cingulate cortex, rather than the whole PFC, that matters. They have a case study that refutes that. Patient R is a man whose brain was devastated by herpes simplex encephalitis, yet survived with normal intelligence and anterograde amnesia (loss of the ability to form new memories). Most importantly to this point, he has retained full self-awareness.

Patient R, aka Roger (Philippi et al. 2012), provides us with a novel angle for assessing certain versions of the NC hypothesis. Roger has extensive damage to his PFC as well as his ACC and insula, bilaterally. He has been probed for self-awareness (SA) in numerous ways, some standard, some novel with positive results for all probes. The authors of the 2012 study concluded that SA is likely a function of the interaction of multiple brain regions, with some redundancy, rather than dependent upon one particular region.8 Roger’s case, like others described in the literature (Damasio et al. 2013), seems to demonstrate fairly conclusively that the PFC, the ACC, and the insula are not needed for SA, including SA of a fairly sophisticated sort, a sort we need not presume animals to have to make our case here.

Patient R also has a normal physical and emotional response to pain — if anything, he now reacts more strongly.

So now if you want to argue for a discrete localization of self-awareness in the brain, you’re either going to have to pick a different brain region or claim that Patient R is a p-zombie. Or, perhaps, that the brain has a lot more flexibility than was thought. I like this last idea, but then, that makes the pursuit of a feature unique to humans futile.

Further, these cases suggest an alternative to the rigid structure-function correlation thesis. Resilience of function following brain damage suggests the existence of degrees of freedom in the relationships between certain functions and neuroanatomical structures (Rudrauf, 2014). Anatomical regions and networks normally supporting central psychological functions (like the emotional appraisal of pain) may simply be the usual defaults. In patients such as Roger, functional resilience after such extensive and irreversible anatomical damage cannot be explained by structural plasticity, in the sense of anatomical restoration or large-scale “rewiring” (e.g., dendritic sprouting and axon regeneration) to restore structural connectivity. Large-scale functional networks supporting key psychological functions, however, can be maintained or restored even when the integrity of normal anatomical networks is massively and irremediably compromised.

This suggests that a different concept of flexibility is more apt, namely what Rudrauf (2014) has called “neurofunctional resilience”. This concept is based on the phenomenon of preserved function in spite of large-scale architectural changes, is not limited to one specific class of mechanisms or levels of observation, and indicates a relative openness in implementation at various levels of a functional hierarchy. The neurofunctional resilience framework, while in need of elaboration and refinement, makes more sense of lesion cases like Roger’s, observed variation in structure-function relationships in imaging studies, interspecific structure-function variations, the relative unimportance of lesion locales versus lesion size vis-à-vis functional deficits in the developing brain (Pascual, 2017, 5; Battro, 2000), and better fits general theoretical considerations about multiple realizability drawn from computational neuroscience. In realizing that a crude, “phrenological” localizationist structure-function paradigm (even one incorporating plasticity) is unable to account for these observable phenomena, one need not, of course, embrace the old holistic, “equipotentiality” theories of brain function (see Finger, 1994, ch., p. 4). A new, subtler approach is needed.

My first thought would have been that Patient R is an amazing example of neuronal plasticity, but the author is right: this is something more impressive. Big chunks of the brain are just gone; minor self-repair mechanisms, like neurons regrowing around a damaged pathway, are not sufficient. This is as if your car had the electronic engine timing system blown off, so the wires were rerouted to make use of circuits in your car radio instead. Be impressed! Brains seem to have a biological imperative to assemble themselves into some kind of cognitively functional structure, in spite of massive damage.

But never mind human brains — they’re too complicated, and you can’t do experiments on them. What about fish brains? Do they feel pain? And what about cephalopods?

As Godfrey-Smith (2016, 94 f.) notes, flexible behaviors and preference changes related to pain avoidance and analgesia-seeking (observed in both fish and chickens) in entirely evolutionarily novel situations and perhaps certain grooming and protecting behaviors associated with bodily damage are arguably best explained in terms of the presence of consciously experienced negative pain affect. And when one considers the overall behavioral, affective, and cognitive repertoire of, for example, cephalopods, as Godfrey-Smith does at length, the notion that such an animal, whose nervous system is so different from ours, does what it does in the absence of consciousness begins to look implausible and continued commitment to it perversely skeptical.

It seems more reasonable to follow the approach of Segner (2012, p. 78) who, in considering fish pain, looks at seven relevant properties: (1) nociceptors, (2) pain related brain structures homologous or analogous to those found in humans, (3) pathways connecting peripheral nociceptors to higher brain regions, (4) endogenous opioids and opioid receptors in the CNS, (5) analgesic-mediated reduction of response to noxious stimuli, (6) complex forms of learning, including avoidance learning of noxious stimuli, and (7) suspension of normal behavior in response to noxious stimuli. Humans and fish, Segner concludes, unequivocally share all but item (2), which is partially shared: we share subcortical structures with fish but not the neocortical structures. However, given the evidence reviewed in this section, it is clear that the neocortical structures commonly thought to be necessary for pain affect are not required in any case (cf., Merker, 2007; Ginsburg & Jablonka, 2019) Surely the other similarities are sufficient to make reasonable the inference to the presence of consciously felt fish pain (cf., Tye, 2017, 91ff.). For mammals, as we have seen, all of these similarities are in place.

That “phrenological” approach doesn’t work well for fish, and even less well for cephalopods which have virtually no homology with our brains. Those seven criteria are a useful rubric for figuring out if a given brain can be aware or feel pain, and like the authors say fish meet all of the criteria except #2, having homologous pain-related brain structures. But we also just saw that Patient R fails to have homologous pain related structures. It would be strange to then assert that an organism that has the other six features would have failed, in its evolutionary history, to have incorporated them into an integrated pain awareness system.

Segner codifies the basic analogy argument for the presence of negative affect in animals that goes beyond the one we all spontaneously draw from our admittedly fallible raw intuitions. On our view, this basic analogy argument coupled with the considerations about neurofunctional resilience (and evolutionary analogies) we have adduced yield a reasonably high probability for the claim that negative pain affect is present in mammals, avians, fish, and cephalopods. Even if we are mistaken about the latter three, however, these considerations make the claim that it is present in mammals so probable that the more ambitious NC thesis of M. Murray and W.L. Craig is cast into nearly insurmountable doubt.

The paper goes on to discuss in detail the specific question of whether fish feel pain (short answer: yes), cetaceans, the issue of blindsight, and much more briefly, consciousness, which would require a stack of books to consider. I’ll stop here, though, disappointed that nowhere does the paper discuss spider pain, or any invertebrates other than cephalopods. Invertebrates are so alien and distantly removed from us that it is nearly impossible to discern a pain affect in them, but they also meet 6 of the 7 Segner criteria. The pain pathways in vertebrate and invertebrate systems also show homology at the molecular level, and it’s possible to see similarites across many phyla.

Maybe that’s for a different day. I’ve been having a fun time lately diving into an area I’ve neglected for a while, developmental neuroscience, and maybe I’ll be motivated to tell you all why you should be kind to bugs, because they have feelings, too, and maybe even experience suffering.