Category Archives: biology

Will the growing deer prion epidemic spread to humans? Why not?

Helpful background reading: What’s the deal with prions?

A novel lethal infectious neurological disease emerged in American deer a few decades ago. Since then, it’s spread rapidly across the continent. In areas where the disease is found, it can be very common in the deer there.

Map from the Cornell Wildlife Health Lab.

Chronic wasting disease isn’t caused by a bacteria, virus, protist, or worm – it’s a prion, which is a little misshapen version of a protein that occurs naturally in the nervous systems of deer.

Chemically, the prion is made of exactly the same stuff as its regular counterpart – it’s a string of the same amino acids in the same order, just shaped a little differently. Both the prion and its regular version (PrP) are monomers, single units that naturally stack on top of each other or very similar proteins. The prion’s trick is that as other PrP moves to stack atop it, the prion reshapes them – just a little – so that they also become prions. These chains of prions are quite stable, and, over time, they form long, persistent clusters in the tissue of their victims.

We know of only a few prion diseases in humans. They’re caused by random chance misfolds, a genetic predisposition for PrP to misfold into a prion, accidental cross-contamination via medical supplies, or, rarely, from the consumption of prion-infected meat. Every known animal prions is a misfold of the same specific protein, PrP. PrP is expressed in the nervous system, particularly in the brain – so infections cause neurological symptoms and physical changes to the structure of the brain. Prion diseases are slow to develop (up to decades), incurable, and always fatal.

There are two known infectious prion diseases in people. One is kuru, which caused an epidemic among tribes who practiced funerary cannibalism in Papua New Guinea. The other is mad cow disease, also known as bovine spongiform encephalopathy (BSE) AKA Variant Creutzfeldt-Jakob disease, which was first seen in humans in 1996 in the UK, and comes from cows.

Chronic wasting disease (CWD)…

Is, like every other animal prion disease, a misfold of PrP. PrP is quite similar in both humans and deer.
Is found in multiple deer species which are commonly eaten by humans.
Can be carried in deer asymptomatically.

But it doesn’t seem to infect people. Is it ever going to? If a newly-emerged virus were sweeping across the US and killing deer, which could be spread through consuming infected meat, I would think “oh NO.” I’d need to see very good evidence to stop sounding the alarm.

Now, the fact that it’s been a few decades, and it hasn’t spread to humans yet, is definitely some kind of evidence about safety. But are we humans basically safe from it, or are we living on borrowed time? If you live in an area where CWD has been detected, should you eat the deer?

Sidenote: Usually, you’ll see “BSE” used for the disease in cows and “VCJ” for the disease in humans. But they’re caused by the same agent and this essay is operating under a zoonotic One Health kind of stance, so I’m just calling the disease BSE here. (As well as the prion that causes it, when I can get away with it.)

In short

The current version of CWD is not infectious to people. We checked. BSE showed that prions can spill over, and there’s no reason a new CWD variant will never do the same. The more cases there are, the more likely it is to spill over. That said, BSE did not spill over very effectively. It was always incredibly rare in humans. It’s an awful disease to get, but the chance of getting it is tiny. Prions in general have a harder time spilling over between species than viruses do. CWD might behave somewhat differently but probably will stay hampered by the species barrier.

Why do I think all of this? Keep reading.

North American elk (wapiti), which can carry CWD. This and the image at the top of the article are adapted from a photo from the Idaho Fish and Game department, under a CC BY 2.0 license.

Prions aren’t viruses

I said before that if a fatal neurological virus were infecting deer across the US, and showed up in cooked infected meat, my default assumption would be “we’re in danger.” But a prion isn’t a virus. Why does that matter?

Let’s look at how they replicate. A virus is a little bit of genetic material in a protein coating. You, a human, are a lot of genetic in a protein coating. When a virus replicates, it slips into your cells, and it hijacks your replication machinery to run its genes instead. Instead of all the useful-to-you tasks your genome has planned, the virus’s genome outlines its own replication, assembles a bunch more viruses, and blows up the factory (cell) to turn them loose into the world.

In other words, the virus using a robust information-handling system that both you and it have in common – the DNA → RNA → protein pipeline often called “the central dogma” of biology. To a first approximation, you can just add any genetic information at all into the viral genome, and as long as it doesn’t interfere with the virus’s process, whatever you add will get replicated in there too.

Prions do not work like this. They don’t tap into the central dogma. What makes them so fundamentally cool is that they replicate without touching the replication machinery that everything else alive uses – their replication is structural, like a snowflake forming. The host provides raw material in the form of PrP, and the prion – once it lands – encourages that material to shape in the right way for more to form atop it.

What this means is that you can’t encode arbitrary information into a prion. This isn’t just a factor – it’s not as though a prion runs on a separate “protein genome” we could decipher and then encode what we like into. The entire structure of the prion has to work together to replicate itself. If you made a prion with some different fold in it, that fold has to not just form a stable protein, but to pass itself along as well. They don’t have a handy DNA replicase enzyme to outsource to – they have to solve the problem of replication themselves, every time.

Prions can evolv e, but they do it less – they have fewer free options, they’re more constrained than a virus would be in terms of changes that don’t interrupt the rest of the refolding process and that on top of that promulgate themselves.

This means that prions are slower to evolve than viruses. …I’m pretty sure, at least. It makes a lot of sense to me. The thing that this definitely means is that:

It’s very hard for prions to cross species barriers

PrP is a very conserved protein across mammals, meaning that all mammals have a version of PrP that’s pretty similar – 90%+ similarity.* But the devil lies in that 10%.

Prions are finely tuned – to convert PrP to a prion, it basically needs to be identical, or at least functionally identical, everywhere the prion works. It not just needs to be susceptible to the prion’s misfolding, it also needs to fold into something that itself can replicate. A few amino acid differences can throw a wrench in the works.

It’s clear that infectious prions can have a hard time crossing species barriers. It depends on the strain. For instance: Mouse prions convert hamster PrP.** Hamster prions don’t convert mouse PrP. Usually a prion strain converts its usual host PrP best, but one cat prion more efficiently converts cow PrP. In a test tube, CWD can convert human or cow PrP a little, but shows slightly more action with sheep PrP (and much more with, of course, deer PrP.)

This sounds terribly arbitrary. But remember, prion behavior comes down to shape. Imagine you’re playing with legos and duplo blocks. You can stack legos on legos and duplos on duplos. You can also put a duplo on top of a lego block. But then you can only add duplo blocks on top of that – you’ve permanently changed what can get added to that stack.

When we look at people – or deer, or sheep, etc – who are genetically resistant to prions (more on that later), we find that serious resistance can be conferred by single nucleic acid changes in the PrP gene. Tweak one single letter of DNA in the right place, and their PrP just doesn’t bend into the prion shape easily. If the infection takes, it proceeds slower – slow enough a person might die of old age before the prion would kill them.

So if a decent number of members of a species can be resistant to prion diseases, based on as little as one amino acid – then a new species, one that might have dozens of different amino acids in the PrP gene, is unlikely to be fertile ground for an old prion.

* (This is kind of weird given that we don’t know what PrP actually does – the name PrP just stands “prion protein” because it’s the protein that’s associated with prions, and we don’t know its function. We can genetically alter mice so that they don’t produce PrP at all, and they show slight cognitive issues but they’re basically fine. Classic evolution. It’s appendices all over again.)

** Sidebar: When we look at studies for this, we see that like a lot of pathology research, there's a spectrum of experiments on different points on the axis from “deeply unrealistic” to “a pretty reasonable simulacrum of natural infection”, like:

1. Shaking up loose prions and PrP in a petri dish and seeing if the PrP converts

2. Intracranial injection with brain matter (i.e. grinding up a diseased brain and injecting some of that nasty juice into the brain of a healthy animal and seeing if it gets sick)

3. Feeding (or some other natural route of exposure) a plausible natural dose of prions to a healthy animal and seeing if that animal gets sick

The experiments mentioned below are based on 1. Only experiments that do 3 actually prove the disease is naturally infectious. For instance, Alzheimer’s disease is “infectious” if you do 2, but since nobody does that, it’s not actually a contagious threat. That said, doing more-abstracted experiments means you can really zoom in on what makes strain specificity tick.

But prions do cross species barriers

Probably the best counterargument to everything above is that another prion disease, BSE, did cross the species barrier. This prion pulled off a balancing act: it successfully infected cows and humans at the same time.

Let’s be clear about one big and interesting thing: BSE is not good at crossing the species barrier. When I say this, I mean two things:

First, people did not get it often. While the big UK outbreak was famously terrifying, only around 200 people ever got sick from mad cow disease. Around 200,000 cows tested positive for it. But most cows weren’t tested. Researchers estimate that 2 million cows total in the UK had BSE, most of which were slaughtered and entered the food chain. These days, Britain has 2 million cows at any given time.

At first glance, and to a first approximation, I think everyone living in the UK for a while between 1985 and 1996 or so (who ate beef sometimes) must have eaten beef from an infected animal. That’s approximately who the recently-overturned blood donation ban in the US affected. I had thought that was sort of an average over who was at risk of exposure – but no, that basically encompassed everyone who was exposed. Exposure rarely leads to infection.

You’re more likely to get struck by lightning than to get BSE even if you have eaten BSE-infected beef.

Second, in the rare cases the disease takes, it’s slower. Farm cows live short lives, and the cows that died from BSE would have gotten old for the beef industry at 4-5 years post-exposure. They survived at most weeks or months after symptoms began. Humans infected with BSE, meanwhile, can harbor it for up to decades post-exposure, and live an average of over a year after showing symptoms.

I think both of these are directly attributable to the prion just being less efficient at converting human PrP – versus the PrP of the cows it was adapted to. It doesn’t often catch on in the brain. When it does, it moves extremely slowly.

But it did cross over. And as far as I can tell, there’s no reason CWD can’t do the same. Like viruses, CWD has been observed to evolve as it bounces between hosts with different genotypes. Some variants of CWD seem more capable of converting mouse PrP than the common ones. The good old friend of those who play god, serial passaging, encourages it.

(Note also that all of the above differs from kuru, which did cause a proper epidemic. Kuru spread between humans and was adapted for spreading in humans. When looking to CWD, BSE is a better reference point because it spread between cows and only incidentally jumped to humans – it was never adapted for human spread.)

How is CWD different from BSE?

BSE appears in very low, very low numbers anywhere outside the brains and spines of its victims. CWD is also concentrated in the brains, but also appears in the spines and lymphatic tissue, and to a lesser but still-present degree, everywhere else: muscle, antler velvet, feces, blood, saliva. It’s more systematic than BSE.

Cows are concentrated in farms, and so are some deer, but wild deer carry CWD all hither and yon. As they do, they leave it behind in:

Feces – Infected deer shed prions in their feces. An animal that eats an infected deer might also shed prions in its feces.
Bodies – Deer aren’t strictly herbivorous if push comes to shove. If a deer dies, another deer might eat the body. One study found that after a population of reindeer started regularly gnawing on each other’s antlers (#JustDeerThings), CWD swept in.
Dirt – Prions are resilient and can linger, viable, in soil. Deer eat dirt accidentally while eating grass, as well as on purpose from time to time and can be infected.
Grass – Prions in the soil or otherwise deposited onto plant tissue can hang out in living grass for a long time.
Ticks – One study found that ticks fed CWD prions don’t degrade the protein. If they’re then eaten by deer (for instance, during grooming), they could spread CWD. This study isn’t perfect evidence; the authors note that they fed the ticks a concentration of prions about 1000x higher than is found in infected deer blood. But if my understanding of statistics and infection dynamics is correct, that suggests that maybe 1 in 1000 ticks feeding on infected deer blood reaches that level of infectivity? Deer have a lot of ticks! Still pretty bad!

That’s a lot of widespread potentially-infectious material.

When CWD is in an area, it can be very common – up to 30% of wild deer, and up to 90% of deer on an infected farm. These deer can carry CWD and have it in their tissues for quite some time asymptomatically – so while it frequently has very visible behavioral and physical symptoms, it also sometimes doesn’t.

In short, there’s a lot of CWD in lots of places through the environment. It’s also spreading very rapidly. If a variant capable of infecting both deer and humans emerged, there would be a lot of chances for possible exposure.

Deer on a New Zealand deer farm. By LBM1948, under a CC BY-SA 4.0 license.

What to do?

As an individual

As with any circumstance at all, COVID or salmonella or just living in a world that is sometimes out to get you, you have to choose what level of risk you’re alright with. At first, writing this piece, I was going to make a suggestion like “definitely avoid eating deer from areas that have CWD just in case your deer is the one that has a human-transmissible prion disease.” I made a little chart about my sense of the relative risk levels, to help put the risk in scale even though it wasn’t quantified. It went like this:

Imagine a spectrum of risk of getting a prion disease. On one end, which we could call "don't do this", is "eating beef from an animal with BSE". Close to that but slightly less risky is "eating deer from an animal with CWD". On the other very safe end is "eating beef from somewhere with known active BSE cases". This entire model is wrong, though.

But, as usual, quantification turns out to be pretty important. I actually did the numbers about how many people ever got sick from BSE (~200) and how many BSE-infected cows were in the food chain (~2,000,000), which made the actual risk clear. So I guess the more prosaic version looks like this:

Remember that spectrum of risk? Well, all of these risks are infinitesimal. Worry about something else! Eating beef from an animal with BSE is still more dangerous than eating deer from an animal with CWD, which is more dangerous than eating beef from somewhere without known active BSE cases - but all of these are clustered very, very far on the safe side of the graph.

…This is sort of a joke, to be clear. There’s not a health agency anywhere on earth that will advise you to eat meat from cows known to have BSE, and the CDC recommends not eating meat from deer that test positive for CWD (though it’s never infected a human before.)

On top of that, the overall threat is still uncertain because what you’re betting on is “the chance that this animal will have had an as-of-yet undetected CWD variant that can infect humans.” There’s inherently no baseline for that!

We don’t know what CWD would act like if it spilled over. It might be more infectious and dangerous than other infectious prion diseases we’ve seen – remember, with humans, the sample size is 2! So if CWD is in your area and it’s not a hardship to avoid eating deer, you might want to steer clear. …But the odds are in your favor.

As a society

There’s not an obvious solution. The epidemic spreading among deer isn’t caused by a political problem, it’s from nature.

The US is doing a lot right: mainly, it is monitoring and tracking the spread of the disease. It’s spreading the word. (If nothing else, you can keep track of this by subscribing to google alerts for “chronic wasting disease”, and then pretty often you’ll get an email saying things like “CWD found in Florida for the first time” or “CWD found an hour from you for the first time.”) It is encouraging people to submit deer heads for testing, and not to eat meat from deer that test positive. The CDC, APHIS, Fish & Wildlife Service, and more are all aware of the problem and participating in tracking it.

What more could be done? Well, a lot of the things that would help a potential spillover of CWD look like actions that can be taken in advance of any threatening novel disease. There is research being done on prions and how they cause disease, better diagnostics, and possible therapeutics. All of these are important. Prion disease diagnosis and treatment is inherently difficult, and on top of that, has little overlap with most kinds of diagnosis or treatment. It’s also such a rare set of diseases that it’s not terribly well studied. (My understanding is that right now there are various kinds of tests for specific prion diseases – which could be adapted for a new prion disease – that are extremely sensitive although not particularly cheap or widespread.)

I don’t know a lot about the regulatory or surveillance situation vis-a-vis deer farms, or for that matter, much about deer farms at all. I do know that they seem to be associated with outbreaks, and heavy disease prevalence once there is an outbreak. That’s a smart area to an eye on.

If CWD did spill over, what would happens?

It will probably also take time to locate cases and identify the culprit, but given the aforementioned awareness and surveillance of the issue, it ought to take way less time than it took to identify the causative agent of BSE. Officials are already paying attention to deaths that could potentially be CWD-related, like neurodegenerative illnesses that kill young people.

First, everyone gets very nervous about eating venison for a while.

After that, I expect the effects will look a lot like the aftermath of mad cow disease. Mad cow disease, and very likely a hypothetical CWD spillover, would not be transmissible between people in usual ways – coughing, skin contact, fomites, whatever.

It is transmissible via unnatural routes, which is to say, blood transfusions. You might remember how people who’d spent over 6 months in Britain couldn’t donate blood in the US until 2022, a direct response to the BSE outbreak. Yes, the disease was extremely rare, but unless you can quickly and cheaply test incoming blood donations, a donor could donate blood to multiple people. Suppose some of them donate blood down the line. You’d have a chain of infection and a disease with a potentially decades-long incubation period. And remember, the disease is incurable and fatal. So basically, the blood donation system (and probably other organ donation) becomes very problematic.

That said, I don’t think it would break down completely. In the BSE case, lots of people in the UK eat beef from time to time – probably most people. But with a deerborne disease, I would guess that a lot of the US population could confidently declare that they haven’t eaten deer within the past, say, year or so (prior to a detected outbreak.) So I think there’d be panic and perhaps strain on the system but not necessarily a complete breakdown. Again, all of this is predicated on a new prion disease working like known human prion diseases.

Genetic resistance

One final fun fact: People who have a certain allele in the PrP gene – specifically, have the genotype PRNP 129M/V or V/V – are incredibly genetically resistant to known infectious prion diseases. If they do get infected, they survive for much longer.

It’s also not clear that this would hold true for a hypothetical CWD crossover to humans. But it is true for both kuru and BSE. It’s also partly (although not totally) protective against sporadic Creutzfeldt-Jakob disease.

If you’ve gotten a service like 23&me, maybe check out your data and see if you’re resistant to infectious prion diseases. Here’s what you’re looking for:

129M/V or V/V (amino acids), or G/G or A/G (nucleotides) – rs1799990

If you instead have M/M (amino acids) or A/A (nucleotides) at that site, you’re ~~SOL~~ at a higher but still very low overall risk.

Final thoughts

I think exercises like “if XYZ disease emerges, what will the ramifications and response be” are valuable. They lead to questions like “what problems will seem obvious in retrospect” and “how can we build systems now that will improve outcomes of disasters.” This is an interesting case study and I might revisit it later.

Has anyone reading this ever been struck by lightning? That’s the go-to comparison for things being rare. But 1 in 15,000 isn’t, like, unthinkably rare. I’m just curious.

No, seriously, what’s the deal with deer farms? I never think about deer farms much. When I think of venison, I imagine someone wearing camo and carrying a rifle out into a national forest or a buddy’s backyard or something. How many deer are harvest from hunting vs. farms? What about in the US vs. worldwide? Does anyone know? Tell me in the comments.

This essay was crossposted to LessWrong. Also linked at the EA Forums.

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There’s no such thing as a tree (phylogenetically)

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So you’ve heard about how fish aren’t a monophyletic group? You’ve heard about carcinization, the process by which ocean arthropods convergently evolve into crabs? You say you get it now? Sit down. Sit down. Shut up. Listen. You don’t know nothing yet.

“Trees” are not a coherent phylogenetic category. On the evolutionary tree of plants, trees are regularly interspersed with things that are absolutely, 100% not trees. This means that, for instance, either:

The common ancestor of a maple and a mulberry tree was not a tree.
The common ancestor of a stinging nettle and a strawberry plant was a tree.
And this is true for most trees or non-trees that you can think of.

I thought I had a pretty good guess at this, but the situation is far worse than I could have imagined.

CLICK TO EXPAND. Partial phylogenetic tree of various plants. TL;DR: Tan is definitely, 100% trees. Yellow is tree-like. Green is 100% not a tree. Sourced mostly from Wikipedia.

I learned after making this chart that tree ferns exist (h/t seebs), which I think just emphasizes my point further. Also, h/t kithpendragon on LW for suggestions on increasing accessibility of the graph.

Why do trees keep happening?

First, what is a tree? It’s a big long-lived self-supporting plant with leaves and wood.

Also of interest to us are the non-tree “woody plants”, like lianas (thick woody vines) and shrubs. They’re not trees, but at least to me, it’s relatively apparent how a tree could evolve into a shrub, or vice-versa. The confusing part is a tree evolving into a dandelion. (Or vice-versa.)

Wood, as you may have guessed by now, is also not a clear phyletic category. But it’s a reasonable category – a lignin-dense structure, usually that grows from the exterior and that forms a pretty readily identifiable material when separated from the tree. (…Okay, not the most explainable, but you know wood? You know when you hold something in your hand, and it’s made of wood, and you can tell that? Yeah, that thing.)

All plants have lignin and cellulose as structural elements – wood is plant matter that is dense with both of these.

Botanists don’t seem to think it only could have gone one way – for instance, the common ancestor of flowering plants is theorized to have been woody. But we also have pretty clear evidence of recent evolution of woodiness – say, a new plant arrives on a relatively barren island, and some of the offspring of that plant becomes treelike. Of plants native to the Canary Islands, wood independently evolved at least 38 times!

One relevant factor is that all woody plants do, in a sense, begin life as herbaceous plants – by and large, a tree sprout shares a lot of properties with any herbaceous plant. Indeed, botanists call this kind of fleshy, soft growth from the center that elongates a plant “primary growth”, and the later growth from towards the outside which causes a plant to thicken is “secondary growth.” In a woody plant, secondary growth also means growing wood and bark – but other plants sometimes do secondary growth as well, like potatoes in their roots.

This paper addresses the question. I don’t understand a lot of the closely genetic details, but my impression of its thesis is that: Analysis of convergently-evolved woody plants show that the genes for secondary woody growth are similar to primary growth in plants that don’t do any secondary growth – even in unrelated plants. And woody growth is an adaption of secondary growth. To abstract a little more, there is a common and useful structure in herbaceous plants that, when slightly tweaked, “dendronizes” them into woody plants.

Dendronization – Evolving into a tree-like morphology. (In the style of “carcinization“.) From ‘dendro‘, the ancient Greek root for tree.

Can this be tested? Yep – knock out a couple of genes that control flower development and change the light levels to mimic summer, and researchers found that Arabidopsis – rock cress, a distinctly herbaceous plant used as a model organism – grows a woody stem never otherwise seen in the species.

The tree-like woody stem (e) and morphology (f, left) of the gene-altered *Aridopsis*, compared to its distinctly non-tree-like normal form (f, right.) Images from Melzer, Siegbert, et al. “Flowering-time genes modulate meristem determinacy and growth form in Arabidopsis thaliana.” *Nature genetics* 40.12 (2008): 1489-1492.

So not only can wood develop relatively easily in an herbal plant, it can come from messing with some of the genes that regulate annual behavior – an herby plant’s usual lifecycle of reproducing in warm weather, dying off in cool weather. So that gets us two properties of trees at once: woodiness, and being long-lived. It’s still a far cry from turning a plant into a tree, but also, it’s really not that far.

To look at it another way, as Andrew T. Groover put it:

“Obviously, in the search for which genes make a tree versus a herbaceous plant, it would be folly to look for genes present in poplar and absent in Arabidopsis. More likely, tree forms reflect differences in expression of a similar suite of genes to those found in herbaceous relatives.”

So: There are no unique “tree” genes. It’s just a different expression of genes that plants already use. Analogously, you can make a cake with flour, sugar, eggs, sugar, butter, and vanilla. You can also make frosting with sugar, butter, and vanilla – a subset of the ingredients you already have, but in different ratios and use.

But again, the reverse also happens – a tree needs to do both primary and secondary growth, so it’s relatively easy for a tree lineage to drop the “secondary” growth stage and remain an herb for its whole lifespan, thus “poaizating.” As stated above, it’s hypothesized that the earliest angiosperms were woody, some of which would have lost that in become the most familiar herbaceous plants today. There are also some plants like cassytha and mistletoe, herbaceous plants from tree-heavy lineages, who are both parasitic plants that grow on a host tree. Knowing absolutely nothing about the evolution of these lineages, I think it’s reasonable to speculate that they each came from a tree-like ancestor but poaized to become parasites. (Evolution is very fond of parasites.)

Poaization: Evolving into an herbaceous morphology. From ‘poai‘, ancient Greek term from Theophrastus defining herbaceous plants (“Theophrastus on Herbals and Herbal Remedies”).

(I apologize to anyone I’ve ever complained to about jargon proliferation in rationalist-diaspora blog posts.)

The trend of staying in an earlier stage of development is also called neotenizing. Axolotls are an example in animals – they resemble the juvenile stages of the closely-related tiger salamander. Did you know very rarely, or when exposed to hormone-affecting substances, axolotls “grow up” into something that looks a lot like a tiger salamander? Not unlike the gene-altered Arabidopsis.

A normal axolotl (left) vs. a spontaneously-metamorphosed “adult” axolotl (right.)

[Photo of normal axolotl from By th1098 – Own work, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=30918973. Photo of metamorphosed axolotl from deleted reddit user, via this thread: https://www.reddit.com/r/Eyebleach/comments/etg7i6/this_is_itzi_he_is_a_morphed_axolotl_no_thats_not/ ]

Does this mean anything?

A friend asked why I was so interested in this finding about trees evolving convergently. To me, it’s that a tree is such a familiar, everyday thing. You know birds? Imagine if actually there were amphibian birds and mammal birds and insect birds flying all around, and they all looked pretty much the same – feathers, beaks, little claw feet, the lot. You had to be a real bird expert to be able to tell an insect bird from a mammal bird. Also, most people don’t know that there isn’t just one kind of “bird”. That’s what’s going on with trees.

I was also interested in culinary applications of this knowledge. You know people who get all excited about “don’t you know a tomato is a fruit?” or “a blueberry isn’t really a berry?” I was one once, it’s okay. Listen, forget all of that.

There is a kind of botanical definition of a fruit and a berry, talking about which parts of common plant anatomy and reproduction the structure in question is derived from, but they’re definitely not related to the culinary or common understandings. (An apple, arguably the most central fruit of all to many people, is not truly a botanical fruit either).

Let me be very clear here – mostly, this is not what biologists like to say. When we say a bird is a dinosaur, we mean that a bird and a T. rex share a common ancestor that had recognizably dinosaur-ish properties, and that we can generally point to some of those properties in the bird as well – feathers, bone structure, whatever. You can analogize this to similar statements you may have heard – “a whale is a mammal”, “a spider is not an insect”, “a hyena is a feline”…

But this is not what’s happening with fruit. Most “fruits” or “berries” are not descended from a common “fruit” or “berry” ancestor. Citrus fruits are all derived from a common fruit, and so are apples and pears, and plums and apricots – but an apple and an orange, or a fig and a peach, do not share a fruit ancestor.

Instead of trying to get uppity about this, may I recommend the following:

Acknowledge that all of our categories are weird and a little arbitrary
Look wistfully of pictures of Welwitschia
Send a fruit basket to your local botanist/plant evolutionary biologist for putting up with this, or become one yourself

While natural selection is commonly thought to simply be an ongoing process with no “goals” or “end points”, most scientists believe that life peaked at *Welwitschia.*

[Photo from By Sara&Joachim on Flickr – Flickr, CC BY-SA 2.0, https://commons.wikimedia.org/w/index.php?curid=6342924 ]

Some more interesting findings:

A mulberry (left) is not related to a blackberry (right). They just… both did that.

[ Mulberry photo by Cwambier – Own work, CC BY-SA 4.0, https://commons.wikimedia.org/w/index.php?curid=63402150. Blackberry photo by By Ragesoss – Own work, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=4496657. ]

Avocado and cinnamon are from fairly closely-related tree species.
It’s possible that the last common ancestor between an apple and a peach was not even a tree.
Of special interest to my Pacific Northwest readers, the Seattle neighborhood of Magnolia is misnamed after the local madrona tree, which Europeans confused with the (similar-looking) magnolia. In reality, these two species are only very distantly related. (You can find them both on the chart to see exactly how far apart they are.)
None of [cactuses, aloe vera, jade plants, snake plants, and the succulent I grew up knowing as “hens and chicks”] are related to each other.
Rubus is the genus that contains raspberries, blackberries, dewberries, salmonberries… that kind of thing. (Remember, a genus is the category just above a species – which is kind of a made-up distinction, but suffice to say, this is a closely-related groups of plants.) Some of its members have 14 chromosomes. Some of its members have 98 chromosomes.
Seriously, I’m going to hand $20 in cash to the next plant taxonomy expert I meet in person. God knows bacteriologists and zoologists don’t have to deal with this.

And I have one more unanswered question. There doesn’t seem to be a strong tend of plants evolving into grasses, despite the fact that grasses are quite successful and seem kind of like the most anatomically simple plant there could be – root, big leaf, little flower, you’re good to go. But most grass-like plants are in the same group. Why don’t more plants evolve towards the “grass” strategy?

Let’s get personal for a moment. One of my philosophical takeaways from this project is, of course, “convergent evolution is a hell of a drug.” A second is something like “taxonomy is not automatically a great category for regular usage.” Phylogenetics are absolutely fascinating, and I do wish people understood them better, and probably “there’s no such thing as a fish” is a good meme to have around because most people do not realize that they’re genetically closer to a tuna than a tuna is to a shark – and “no such thing as a fish” invites that inquiry.

(You can, at least, say that a tree is a strategy. Wood is a strategy. Fruit is a strategy. A fish is also a strategy.)

At the same time, I have this vision in my mind of a clever person who takes this meandering essay of mine and goes around saying “did you know there’s no such thing as wood?” And they’d be kind of right.

But at the same time, insisting that “wood” is not a useful or comprehensible category would be the most fascinatingly obnoxious rhetorical move. Just the pinnacle of choosing the interestingly abstract over the practical whole. A perfect instance of missing the forest for – uh, the forest for …

…

… Forget it.

Timeless Slate Star Codex / Astral Codex Ten piece: The categories were made for man, not man for the categories.

Towards the end of writing this piece, I found that actual botanist Dan Ridley-Ellis made a tweet thread about this topic in 2019. See that for more like this from someone who knows what they’re talking about.

For more outraged plant content, I really enjoy both Botany Shitposts (tumblr) and Crime Pays But Botany Doesn’t (youtube.)

[Crossposted to Lesswrong.]

Naked mole-rats: A case study in biological weirdness

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Epistemic status: Speculative, just having fun. This piece isn’t well-cited, but I can pull up sources as needed – nothing about mole-rats is my original research. A lot of this piece is based on Wikipedia.

When I wrote about “weirdness” in the past, I called marine invertebrates, archaea viruses, and Florida Man stories “predictably weird”. This means I wasn’t really surprised to learn any new wild fact about them. But there’s a sense in which marine invertebrates both are and aren’t weird. I want to try operationalizing “weirdness” as “amount of unpredictability or diversity present in a class” (or “in an individual”) compared to other members of its group.

So in terms of “animals your hear about” – well, you know the tigers, the mice, the bees, the tuna fish, the songbirds, whatever else comes up in your life. But “deep sea invertebrates” seems to include a variety of improbable creatures – a betentacled neon sphere covered in spikes, a six-foot long disconcertingly smooth and flesh-colored worm, bisexual squids, etc. Hey! Weird! That’s weird.

But looking at a phylogenetic tree, we see really quickly that “invertebrates” represent almost the entire animal tree of life.

Image from Telford et al (2015).

Invertebrates represent most of the strategies that animals have attempted on earth, and certainly most of the animals on earth. Vertebrates are the odd ones out.

But you know which animals are profoundly weird, no matter which way you look at it? Naked mole rats. Naked mole-rats have like a dozen properties that are not just unusual, not just strange, but absolutely batshit. Let’s review.

1. They don’t age

What? Well, for most animals, their chance of dying goes up over time. You can look at a population and find something like this:

Mole-rats, they have the same chance of dying at any age. Their graph looks like this:

They’re joined, more or less, by a few species of jellyfish, flatworms, turtles, lobsters, and at least one fish.

They’re hugely long-lived compared to other rodents, seen in zoos at 30+ years old compared to the couple brief years that rats get.

2. They don’t get cancer

Cancer generally seems to be the curse of multicellular beings, but naked mole-rats are an exception. A couple mole-rats have developed cancer-like growths in captivity, but no wild mole-rat has ever been found with cancer.

3. They don’t feel some forms of pain

Mole-rats don’t respond to acid or capsaicin, which is, as far as I know, unique among mammals.

4. They’re eusocial

Definitely unique among mammals. Like bees, ants, and termites, naked mole-rats have a single breeding “queen” in each colony, and other “worker” individuals exist in castes that perform specific tasks. In an evolutionary sense, this means that the “unit of selection” for the species is the queen, not any individual – the queen’s genes are the ones that get passed down.

They’re also a fascinating case study of an animal whose existence was deduced before it was proven. Nobody knew about eusocial mammals for a long time. In 1974, entomologist Richard Alexander, who studied eusocial insects, wrote down a set of environmental characteristics he thought would be required for a eusocial mammal to evolve. Around 1981 and the next decade, naked mole-rats – a perfect match for his predictions – were found to be eusocial.

5. They don’t have fur

Obviously. But aside from genetic flukes or domesticated breeds, that puts them in a small unlikely group with only some marine mammals, rhinoceros, hippos, elephants, one species of boar, and… us.

You and this entity have so much in common.

6. They’re able to survive ridiculously low oxygen levels

It uses very little oxygen during normal metabolism, much less than comparable-sized rodents, and it can survive for hours at 5% oxygen (a quarter of normal levels.)

7. Their front teeth move back and forth like chopsticks

I’m not actually sure how common this is in rodents. But it really weirded me out.

8. They have no regular sleep schedule

This is weird, because jellyfish have sleep schedules. But not mole-rats!

9. They’re cold-blooded

They have basically no ability to adjust their body temperature internally, perhaps because their caves tend to be rather constant temperatures. If they need to be a different temperature, they can huddle together, or move to a higher or lower level in their burrow.

All of this makes me think that mole-rats must have some underlying unusual properties which lead to all this – a “weirdness generator”, if you will.

A lot of these are connected to the fact that mole rats spend almost their entire lives underground. There are lots of burrowing animals, but “almost their entire” is pretty unusual – they don’t surface to find food, water, or (usually) mates. (I think they might only surface when digging tunnels and when a colony splits.) So this might explain (8) – no need for a sleep schedule when you can’t see the sun. It also seems to explain (5) and (9), because thermoregulation is unnecessary when they’re living in an environment that’s a pretty constant temperature.

It probably explains (6) because lower burrow levels might have very little oxygen most of the time, although there’s some debate about this – their burrows might actually be pretty well ventilated.

And Richard Alexander’s 12 postulates that would lead to a eusocial vertebrate – plus some other knowledge of eusociality – suggests that this underground climate, when combined with the available lifestyle and food source of a molerat, should lead to eusociality.

It might also be the source of (2) and (3) – people have theorized that higher CO2 or lower oxygen levels in burrows might reduce DNA damage or related to neuron function or something. (This would also explain why only mole-rats in captivity have had tumors, since they’re kept at atmospheric oxygen levels.) These still seem to be up in the air, though. Mole-rats clearly have a variety of fascinating biochemical tricks that are still being understood.

So there’s at least one “weirdness generator” that leads to all of these strange mole-rat properties. There might be more.

I’m pretty sure it’s not the chopstick teeth (7), at least – but as with many predictions one could make about mole rats, I could easily be wrong.

To watch some naked mole-rats going about their lives, check out the Pacific Science Center’s mole-rat live camera. It’s really fun, if a writhing mass of playful otters that are also uncooked hotdogs sounds fun to you.

Small animals have enormous brains for their size

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One thing that surprised me when working on How Many Neurons Are There was the number of neurons in the brains of very small animals.

Let’s look a classic measurement, the brain-mass:body-mass ratio.* Smarter animals generally have larger brain sizes for their body mass, compared to animals of similar size. Among large animals, humans have famously enormous brains for our size – the highest of any large animal, it seems. But as we look at smaller animals, that ratio goes up again. A mouse has a comparable brain:body-mass ratio to a human. Getting even smaller, insects have higher brain:body-mass ratios than any vertebrate we know of: more like 1 in 6.

But brain mass isn’t quite what we want – brains are mostly water, and there are a lot of non-neuron cells in brains. Conveniently, I also have a ton of numbers put together on number of neurons. (Synapse counts might be better, but those are hard to come by for different species. Ethology would also be interesting.)

And the trend is also roughly true for neuron-count:body-mass. Humans do have unusually high numbers of neurons per kilogram than other animals, but far, far fewer than, for instance, a small fish or an ant.

If you believe some variation on one of the following:

Different species have moral worth in proportion to how many neurons they have
Different animal species have moral worth in proportion to how smart they are
Different species have moral worth in proportion to the amount of complex thought they can do
Different species have moral worth in proportion to how much they can learn**

…then this explanation is an indication that insects and other small animals have much more moral worth than their small size suggests.

How much more?

Imagine, if you will, a standard 5-gallon plastic bucket.

Now imagine that bucket contains 300,000 ants – about two pounds.*** Or a kilogram, if you prefer.

Imagine the bucket. Imagine the equivalent of a couple large apples inside it.

A bucket. Two pounds of ants.

Those ants, collectively, have as many neurons as you do.

(Graphic design is my passion.)

You may notice that an adult human brain actually weighs more than two pounds. What’s going on? Simply, insect brains are marvels of miniaturization. Their brains have a panoply of space-saving tricks, and the physical cells are much smaller.

🐜🐜🐜

*Aren’t the cool kids using cephalization quotients rather than brain-mass:body-mass ratios? Yes, when it comes to measurements of higher cognition in vertebrates, cephalization is (as far as I’m aware) thought of as better. But there’s debate about that too. Referring to abilities directly probably makes sense for assessing abilities. I don’t know much about this and it’s not the focus of this piece, anyway.

**Yes, I know that only the first question is directly relevant to this piece, and that all of the others are different. I’m just saying it’s evidence. We don’t have a lot of behavioral data on small animals anyways, but I think we can agree there’s probably a correlation between brain size and cognitive capacity.

***Do two pounds of “normal-sized” ants actually fit in a five-gallon bucket? Yes. I couldn’t find a number for “ant-packing density” in the literature, but thanks to the valiant efforts of David Manheim and Rio Lumapas, it seems to be between 0.3 gallons (5 cups) and 5.5 gallons. It depends on size and whether ants pack more like spheres or more like blocks.

🐜🐜🐜

Suggested readings: Brian Tomasik on judging the moral importance of small minds (link is to the most relevant part but the whole essay is good) and on “clock speeds” in smaller animal brains, Suzana Herculano-Houzel on neuron count and intelligence in elephants versus humans, How many neurons are there. (The last piece also contains most of the citations for this week. Ask if you want specific ones.)

This piece is crossposted to the Effective Altruism Forum.

Spaghetti Towers

Biodiversity for heretics

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Epistemic status: Not very confident in my conclusions here. Could be missing big things. Information gained through many hours of reading about somewhat-related topics, and a small few hours of direct research.

Summary: Biodiversity research is popular, but interpretations of it are probably flawed, in that they’re liable to confuse causation and correlation. Biodiversity can be associated with lots of variables that are rarely studied themselves, and one of these, not “biodiversity” in general, might cause an effect. (For example, more biodiverse ecosystems are more likely to include a particular species that has significant effects on its own.) I think “biodiversity” is likely overstudied compared to abundance, biomass, etc., because it’s A) easier to measure and B) holds special and perhaps undue moral consideration.

From what I was told, biodiversity – the number of species present in an environment – always seemed to be kind of magical. Biodiverse ecosystems are more productive, more stable over time, produce higher crop yields, and are more resistant to parasites and invaders. Having biodiversity in one place increases diversity in nearby places, even though diversity isn’t even one thing (forgive me for losing my citation here). Biodiverse microbiomes are healthier for humans. Biodiversity is itself the most important metric of ecosystem health. The property “having a suite of different organisms living in the same place” just seems to have really incredible effects.

First of all – quickly – some of what I was told isn’t actually true. More diverse microbiomes in bodies aren’t always healthier for humans or more stable. The effects of losing species in ecosystems varies a ton. More biodiverse ecosystems don’t necessarily produce more biomass.

That said, there’s still plenty of evidence that biodiversity correlates with something.

But: biodiversity research and its interpretations have problems. Huston (1997) introduced me to a few very concrete ways this can turn up misleading or downright inaccurate results.

Our knowledge about biodiversity’s effects on ecosystems comes from either experiments, in which biodiversity is manipulated in a controlled setting; or in observations of existing ecosystems. Huston identifies a few ways that these have, historically, given us bad or misleading data:

Biotic or abiotic conditions, either in observations or experiments, are altered between groups. (E.g. you pick some sites to study that are less and more biodiverse, but the more-biodiverse sites are that way because they get more rainfall – which obviously is going to have other impacts)
Species representing the “additional biodiversity” in experiments aren’t chosen randomly, they’re known to have some ecosystem function.
Increasing the number of species increases the chance that one or a few of the added species will have some notable ecosystem effect on their own.

I’m really concerned about (3).

To show why, let’s imagine aliens who come to earth and want to study how humans work. They abduct random humans from across the world and put them in groups of various sizes.

Building walls

The aliens notice that the human civilizations have walls. They give their groups of abducted humans blocks and instruct them to build simple walls.

It turns out that larger groups of humans can build, on average, proportionally longer walls. The aliens conclude that wall-building is a property of larger groups of humans.

Building radios

The aliens also notice that human civilizations have radios. They give their groups of abducted humans spare electronic parts, and instruct them to build a radio.

Once again, it turns out that larger groups of humans are proportionally more likely to be able to build a radio. The aliens conclude that radio-building, too, is a property of large groups of humans.

The mistake the aliens are making is in assuming that wall- and radio-building are functions of “the number of humans you have in one place”. More people can build a longer simple wall, because there’s more hands to lift and help. But when it comes to building radios, a larger group just increases the chance that at least one human in the group will be an engineer.

To the aliens, who don’t know about engineers, “number of humans” kind of relates to the thing they’re interested in – they will notice a correlation – but they’re making a mistake by just waving their hands and saying that mostly only large groups of humans possess the intelligence needed to build a radio, perhaps some sort of hivemind.

Similarly, we’d make a mistake by looking at all the strange things that happen in diverse ecosystems, and saying that these are a magical effect that appears whenever you get large numbers of different plants in the same field. I wonder how often we notice that something correlates with “biodiversity” and completely miss the actual mechanism.

Aside from a specific species or couple of species in combination that have a particular powerful effect on ecosystems, what else might biodiversity correlate to that’s more directly relevant? How about abundance (the number of certain organisms of some kind present)? Or biomass (the combined weight of organisms)? Or environmental conditions, like the input of energy? Or the amount of biomass turnover, or the amount of predation, etc., etc.?

I started wondering about this while doing one of my several projects that relate to abundance in nature. We should still study biodiversity, sure. But the degree to which biodiversity has been studied compared to, say, abundance, has lead us to a world where we know there are 6,399 species of mammals, but nobody has any idea – even very roughly – how many mammals there are. Or how we’re pretty sure that there are about 7.7 million species of animals, plus or minus a few hundred thousand, which is a refinement of many previous estimates of the same thing – and then we have about two people (one of whom is wildly underqualified) trying to figure out how many animals there are at all.

It’s improving. A lot of recent work focuses on functional biodiversity. This is the diversity of properties of organisms in an environment. Instead of just recording the number of algae species in a coastal marine shelf, you might notice that some algae crusts on rocks, some forms a tall canopy, some forms a low canopy, and some grows as a mat. It’s a way of separating organisms into niches and into their interactions with the environment.

Functional diversity seems to better describe ecosystem effects than diversity alone (as described e.g. here). That said, it still leaves the door open for (3) – looking at functional diversity means you must know something about the ecosystem, but it’s not enough to tell you what’s causing the effect in and of itself.

To illustrate why:

Every species has some functional properties that separate it from other species – some different interactions, some different niche or physical properties, etc. We can imagine increasing biodiversity, then, as “a big pile of random variables.”

It turns out that when you start with a certain environment and slowly add or remove “a big pile of random variables”, that changes the environment’s properties. Who would have thought?

So is biodiversity instrumentally relevant to humans?

There are sometimes solid explanations for why biodiversity itself might be relevant to ecosystems, e.g. the increased selection for species complementary over time theory.
Biodiversity probably correlates to the things that studies claim it correlates to, including the ones that find significant environmental effects. I just claim that often, biodiversity is plausibly falsely described as the controlling variable rather than one of its correlates. (That said, there are reasons we might expect people to overstate its benefits – read on.)

If this is true, and biodiversity itself isn’t the driving force we make it out to be, why does everyone study it?

Firstly, I think biodiversity is easier to measure than, say, individual properties, or abundance. Looking at the individual properties and traits of each species in the environment is its whole own science, specific to that particular species and that particular environment. It would be a ridiculous amount of work.

But when we try to get the measure of an ecosystem without this really deep knowledge, we turn into the alien scientists – replacing a precise and intricate interaction with a separate but easier-to-measure variable that sort of corresponds with the real one.

What about studying one of the other ecosystem properties, like abundance? I’m guessing that in the modern research environment, you’d basically have to be collecting biodiversity data anyways.

Researcher: We found 255 beetles in this quadrant!

PI: What kind?

Researcher: You know. Beetles.

…And if you’re identifying everything you find in an environment anyways, it’s easier to just keep track of how many different things you find, rather than do that plus exhaustively search for every individual.

This is just speculation, though.

Secondly, a lot of people believe that species and ecosystems are a special moral unit (independent of any effects or benefits they might have on humans). That’s why people worry about losing the parasites of endangered species, or wonder if we shouldn’t damage biodiversity by eradicating diseases.

And… it’s hard to explain why this seems wrong to me, but I’ll try. I get it. Environmentalism is compelling and widespread. It was the background radiation of virtually almost every interaction with nature I had growing up. It was taken for granted that every drop of biodiversity was a jewel with value beyond measure, that endangered species were inherently worth going to great lengths to protect and preserve, that ecosystems are precariously balanced configurations that should be defended as much as possible from encroachment by humans. Under this lens, of course the number of species present is the default measurement – the more biodiversity preserved from human destruction, the more intricate and elaborate the ecosystem (introduced species excepted), the better.

And… doesn’t that seem a little limited? Doesn’t that seem like a sort of arbitrary way to look at huge parts of the world we live in? It’s not worth throwing out, but perhaps it deserves a little questioning. Where else could we draw the moral lines?

Personally, I realized my morality required me to treat animals as moral patients. This started with animals directly used by humans, but then got me re-examining the wild animals I’d been so fond of for so long.

Currently, I put individual animals and species in mostly-separated mental buckets. A species, a particular pattern instantiated by evolution acting on rocks and water over time, is important – but it’s important because it’s beautiful, like a fantastic painting made over decades by a long-dead artist. We value aesthetics, and interpretations, and certainly the world would be worse off without a piece of beauty like this one.

But an individual matters morally because it feels. It cares, it thinks, it feels joy, it suffers. We know because we are one, and because the same circuits and incentives that run in our brains also run in the brains of the cats, chickens, songbirds, insects, earthworms, whale sharks, and bristlemouths that we share this lonely earth with.

We might say that a species “suffers” or “is in pain”, the same way that a city “is in pain”, and we might mean several different things by that. We might say many of the individuals in the collective suffer. Or we might mean that the species is degraded somehow the way art is degraded – lessened in quantity, less likely to survive into the future, changing rapidly, etc. But it seems like a stretch to call that pain, in the way that being eaten alive is pain.

Obviously, at some point, you have to make trade-offs over what you care about. I don’t have my answers worked out yet, but for now, I put a lot more value on the welfare of individual animals than I used to, and I care less about species.

I don’t expect this viewpoint to become widespread any time soon. But I think it’s possible that the important things in nature aren’t the ones we’ve expected, and that under other values, properties like abundance and interactions deserve much more attention (compared to biodiversity) than they have now.

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[OPEN QUESTION] Insect declines: Why aren’t we dead already?

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One study on a German nature reserve found insect biomass (e.g., kilograms of insects you’d catch in a net) has declined 75% over the last 27 years. Here’s a good summary that answered some questions I had about the study itself.

Another review study found that, globally, invertebrate (mostly insect) abundance has declined 35% over the last 40 years.

Insects are important, as I’ve been told repeatedly (and written about myself). So this news begs a very important and urgent question:

Why aren’t we all dead yet?

This is an honest question, and I want an answer. (Readers will know I take catastrophic possibilities very seriously.) Insects are among the most numerous animals on earth and central to our ecosystems, food chains, etcetera. 35%+ lower populations are the kind of thing where, if you’d asked me to guess the result in advanced, I would have expected marked effects on ecosystems. By 75% declines – if the German study reflects the rest of the world to any degree – I would have predicted literal global catastrophe.

Yet these declines have been going on for apparently decades apparently consistently, and the biosphere, while not exactly doing great, hasn’t literally exploded.

So what’s the deal? Any ideas?

Speculation/answers welcome in the comments. Try to convey how confident you are and what your sources are, if you refer to any.

(If your answer is “the biosphere has exploded already”, can you explain how, and why that hasn’t changed trends in things like global crop production or human population growth? I believe, and think most other readers will agree, that various parts of ecosystems worldwide are obviously being degraded, but not to the degree that I would expect by drastic global declines in insect numbers (especially compared to other well-understood factors like carbon dioxide emissions or deforestation.) If you have reason to think otherwise, let me know.)

Sidenote: I was going to append this with a similar question about the decline in ocean phytoplankton levels I’d heard about – the news that populations of phytoplankton, the little guys that feed the ocean food chain and make most of the oxygen on earth, have decreased 40% since 1950.

But a better dataset, collected over 80 years with consistent methods, suggests that phytoplankton have actually increased over time. There’s speculation that the appearance of decrease in the other study may have been because they switched measurement methods partway through. An apocalypse for another day! Or hopefully, no other day, ever.

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2 extremely literal introspection techniques

The Blue Field Entopic Phenomena

Stare up at a clear blue sky. (If no blue sky is available, for instance, if you’re in Seattle and it’s January, I was able to get a weaker version by putting my face close to this image instead. Your mileage may vary.)

Animation of the phenomena. Made by Wikimedia user Unmismoobjectivo, under a CC BY-SA 3.0 license.

Notice tiny white spots with dark tails darting around your field of vision? You’re looking at your own immune system – those are white blood cells moving in the capillaries in your retina. Normally transparent, they reflect blue light. The darker tails are build-ups of smaller red blood cells in the narrow capillaries, which are all but blocked by the large white blood cells.

This is clear enough that the speed at which the dots move can be used to accurately measure blood pressure in the retina. To do this, patients compare their blue field entopic phenomena to animated dots moving at various speeds. I wanted to find some calibrated gifs to try this at home, so if you see some, let me know.

On the other hand, if you see things that look like this all the time everywhere, it might be visual snow.

2. The Purkinje Tree

WARNING: A cell phone flashlight probably isn’t strong enough to damage your eyes, but especially if you try this with anything stronger than that, or if you have a condition that would make it very bad to accidentally shine a flashlight in your face, use your own judgement on proceeding.

Stand or lie down in a dark room.

Turn on your phone flashlight or a penlight, and hold it up against the side of your face.

Position yourself so that you’re looking into darkness, and the light beam passes just over the front of your eyes – you’re trying to get light to go across the surface of your pupil, but not directly into your eyes.

You might need to adjust the angle.

What you’re looking for is the Purkinje tree – shadows of the retinal blood vessels cast onto other parts of the retina. It was first seen by legendary Czech anatomist Jan Evangelista Purkynê, who also found Purkinje brain cells, sweat glands, and Purkinje fibers in the heart, and introduced the terms “blood plasma” and “protoplasm”.

The Purkinje Tree reminded me of aerial photos of branching riverbeds, as in this NASA photo of the Yarlung Tsangpo River in Tibet. So look for a structure like this.

Once you see it, the image will vanish quickly – your brain already gets an image of the blood vessels on the retina, so it’s used to removing it from your perception and will adapt. If you waggle the light source gently at about one hertz (once per second), the image stays visible.

Happy new year from Eukaryote Writes Blog!

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The children of 3,500,000,000 years of evolution

How many neurons are there?

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Image from NOAA, in the public domain.

Last updated on March 16, 2018. I just finished a large project trying to estimate that. I’ve posted it on its own page here. Here’s the abstract:

We estimate that there are between 10^23 and 10^24 neurons on earth. Most of this is distributed roughly evenly among small land arthropods, fish, and nematodes, or possibly dominated by nematodes with the other two as significant contenders. For land arthropods, we multiplied the apparent number of animals on earth by mostly springtail-sized animals, with some small percentage being from larger insects modeled as fruit flies. For nematodes, we looked at studies that provide an average number of nematodes per square meter of soil or the ocean floor, and multiplied them by the number of neurons in Caenorhabditis elegans, an average-sized nematode. For fish, we used total estimates of ocean fish biomass, attributed some to species caught by humans, and used two different ways of allocating the remaining biomass. Most other classes of animal contribute 10^22 neurons at most, and so are unlikely to change the final analysis. We neglected a few categories that probably aren’t significant, but could conceivably push the estimate up.

Using a similar but less precise process based on evolutionary history and biomass over time, we also estimate that there have been between 10^32 and 10^33 neuron-years of work over the history of life, with around an order of magnitude of uncertainty.

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