Compromise and Conceit

January 23, 2020

26 Responses to “Initial Estimates of the Danger of the Novel Coronavirus in Wuhan, China”

1. Goldo Says:

   
   January 24, 2020 at 6:12 am

   Excuse, I will let any hype I want to scare me thank you very much.
   Also I had had the sex before! how dare you!
2. faustusnotes Says:

   
   January 24, 2020 at 11:57 am

   You do you Goldo! But remember, animals don’t count!
3. Peter Thomson Says:

   
   January 24, 2020 at 12:15 pm

   Thanks for this. Query: I have read that the most virulent strains of a pathogen are favoured in the first irruption into a population lacking immunity. If so, does this happen at the outset or does it take place as the infection spreads? If the latter, very early and stringent intervention would be the way to go.
4. faustusnotes Says:

   
   January 24, 2020 at 1:26 pm

   Actually Peter T I’ve read that too, though I’m not sure if it’s because they’re more virulent or because the population adapts and so they become less virulent over time. And I don’t know if that is an adaptive thing or something that occurs at the outset. I guess in either case, since the population has no immunity and you don’t know the bet cures, it’s better to intervene early and with stringent measures. But that risks what happened with H1N1, where you put in place many measures that are quite socially disruptive for a disease that ultimately is no worse than common influenza. This is a general problem with novel disease outbreaks – you have to balance the social disruption of overreaction against the possible consequences of inaction.

   I should add here too that the news this morning puts the number of deaths at 25, so probably the headline conclusion of my analysis should be that it is between 5 and 15 times as dangerous as common influenza, with the possibility of being as dangerous as Spanish influenza. That’s quite alarming! But, we should wait for updates on the number of confirmed infections before jumping to conclusions.
5. Peter Thomson Says:

   
   January 24, 2020 at 2:20 pm

   I read it in the context of the great plagues that periodically swept Eurasia and killed of a high proportion of Amerindians. The theory was that it’s an adaptive thing – the strains that convert the host body into new pathogens asap do best; then, as immunity spreads, endemic forms are favoured. The measles was deadly in the Americas.
6. faustusnotes Says:

   
   January 24, 2020 at 4:33 pm

   Peter T that’s an interesting point and it got me wondering – what is the evidence for the idea that plagues killed a large proportion of native Americans? By this I don’t mean that the idea is wrong, I just wonder where it comes from? A brief google reveals a lot of people citing some obscure references which contain a lot of unsupported numbers – I found one reference which gives a huge range of numbers to the pre-invasion population. A recent study in PNAS suggests that after contact with Europeans the native American population of all America (North and South) temporarily declined by 50% but this is due to all causes – not just disease but also war. The worst disease that the Europeans brought was Smallpox, with a CFR of about 30%. But what is the rate of spread of smallpox in native American populations that are widely dispersed and don’t interact? How long did it take Smallpox to spread across the whole continent? I assume it could not have spread much faster than the spread of white invaders (since they were bringing it), which makes me think that actually there was a lot of violence at the same time as the Smallpox. When white thugs are murdering your kids on contact they aren’t going to die of smallpox are they? And measles in European populations has a CFR of 0.2% – how much worse is it in a population with no immunity? Passive immunity (inherited from infected parents) in children wears off after a few months, so is it really the case that western populations are “immune” to measles, relative to a population that never experienced it? Recall that the primary contact with a population that had never experienced measles occurred in 1492, when science wasn’t exactly great. Claims that these diseases wiped out half the population assume that those people back in 1492 knew what the population was. How did these people who thought they’d arrived in India estimate the population? What epidemiological assessments did they do after smallpox arrived? Also when did smallpox arrive – one assumes the people on the ships didn’t have it, maybe Smallpox was only a problem after native Americans had been slaughtered and moved onto reservations? This isn’t to say I think disease didn’t do anything, but I wonder at the role of this factor in the population decline.

   The reason I question this is that I have seen a lot of this kind of idea going around in the past 5-10 years and did not really see it further back in time. There is a revisionist attack on the whole idea of genocide, at least in Australia (led by the execrable Windschuttle and his enabler JW Howard), and it makes their job a lot easier if they can say “see it wasn’t our fault, it was mostly disease”. So I would be very suspicious about these ideas. How much of our “understanding” of the biology of the spread of disease in “naive” populations is based on a colonialist’s understanding of people who he thought were so beneath him he couldn’t be bothered to count them.

   (On a related note, I’ve been wondering recently about the idea that cats in Oz are especially bad for native wildlife because the native wildlife “didn’t evolve to be scared of them”. They certainly are scared of humans and Tasmanian Devils and local predators, why would they just sit there when a cat rocks up like it’s their friend? Has anyone ever seen this happen? It sounds like a bunch of excuses for the fact that humans are wiping out native animals).
7. Peter T Says:

   
   January 25, 2020 at 7:36 am

   On the Americas, the diseases spread ahead of European contact – they hit Tenochtitlan before Cortez arrived (we know this from Aztec records), and archaeology shows high mortality among the Incas before Pizzarro. William McNeill’s Plagues and Peoples came out in 1976.

   As with cats, it’s not one or the other. Introduced predators couple with land clearing and introduced competitors to reduce native animal populations and make recovery hard. Diseases couple with conquest and dispossession.

   I’m not an expert, but on my reading CFRs are much much worse in the first impacts on non-immune populations.
8. J-D Says:

   
   January 25, 2020 at 8:06 am

   ‘But remember, animals don’t count!’

   I take it you’re one of the Clever Hans doubters?
9. J-D Says:

   
   January 25, 2020 at 8:30 am

   ‘For the sake of easy writing, let’s call this new disease Dolphin Flu’

   Wouldn’t WCV be even easier to write?
10. faustusnotes Says:

    
    January 25, 2020 at 9:40 pm

    J-D, what’s the fun in writing WCV? I’m not sure who Clever Hans is but I’m scared to google it.

    Peter T, I understand what you’re saying but my question – just thought about for the first time now – is, is any of this verified? A lot of accounts seem to be basically just a christian invader giving their impressions. William McNeil’s Plagues and Peoples you say came out in 1976 – what do you think the quality of demographic research on indigenous mortality from the 15th century was back then? It makes me suspicious. And the PNAS article I link to suggests a 50% reduction in population at that time, which includes war, disease and the demographic effects of both – whereas a book introduction I found suggests a 95% reduction in indigenous population.

    So I wonder, do we actually have any evidence to support this idea? It’s a super convenient idea for genocide denialism, but does it have any basis in data?
11. J-D Says:

    
    January 26, 2020 at 1:09 pm

    J-D, what’s the fun in writing WCV?

    First it was ‘easy writing’, now it’s ‘fun’. Get your priorities straightened out!

    I’m not sure who Clever Hans is but I’m scared to google it.

    Then do what I do and use DuckDuckGo instead. Or you could just look at the Wikipedia article on Clever Hans.

    I’ll give you a couple of clues: the question is not ‘Who is Clever Hans?’ but ‘What was Clever Hans?’; there were reports that Clever Hans could count, but in fact he couldn’t. (You see, I too am one of the Clever Hans doubters.)
12. J-D Says:

    
    January 26, 2020 at 3:34 pm

    But what is the rate of spread of smallpox in native American populations that are widely dispersed and don’t interact?

    What’s the basis for conclusions about how widely dispersed they were and how much they interacted?

    How long did it take Smallpox to spread across the whole continent? I assume it could not have spread much faster than the spread of white invaders (since they were bringing it), …

    Are you justified in assuming that it was spread only by direct contact with Europeans and not by contact between Indigenous groups?

    And measles in European populations has a CFR of 0.2% – how much worse is it in a population with no immunity? Passive immunity (inherited from infected parents) in children wears off after a few months, so is it really the case that western populations are “immune” to measles, relative to a population that never experienced it?

    If degree of resistance to measles is a phenotypic characteristic which is at least partly under the influence of genetic variation (and why wouldn’t it be?), then wouldn’t you expect that a population which has been repeatedly exposed to measles epidemics over a period of centuries will have a significantly higher degree of resistance than a population experiencing measles outbreaks for the first time, as a result of the ordinary processes of natural selection?

    William McNeil’s Plagues and Peoples you say came out in 1976 – what do you think the quality of demographic research on indigenous mortality from the 15th century was back then? It makes me suspicious.

    I think the reason Peter T cited the work of McNeill (not McNeil) was to respond to your remark about your scepticism being founded in having heard about this kind of thing for five to ten years, but not more. I haven’t read Plagues And Peoples but I have read McNeill’s The Rise Of The West, which came out even earlier, in 1963, and McNeill was emphasising the role of disease in history even then, and referring not just to its role in the context of European expansion since 1500 but also to its effect in the context of what he called ‘the closure of the Eurasian ecumene’ a millennium and a half earlier (in other words, very roughly, as best I recall, increased contact between the Roman, Chinese, and other contemporary empires produced increased flow of epidemic disease between them, with serious demographic and then corollary political, economic, and social impacts).

    Of course, McNeill may have been wrong about some of this (in a book of the scale and scope of The Rise Of The West, he must have been wrong about some things, and some of them have probably been exposed by over half a century of subsequent research). The points demonstrated are:
    (1) this idea isn’t as recent an invention as you might suppose; (2) it isn’t something deployed only to exculpate European imperialists/colonisers.
13. Peter Thomson Says:

    
    January 26, 2020 at 7:03 pm

    Faustus

    In Eurasia, plagues generally start in China (sometimes India) and go west. Because these two are the largest clots of humanity on the planet. Tracking mortality in ancient times (say, for the Periclean, 3rd century or Justinian outbreaks) is tricky due to lack of surviving records. Archaeological field surveys, rebuilding of city walls to reflect population losses and cemetery finds all help, but the estimates have a wide range. Medieval sources are a bit better: manorial rolls, monastery records, tax rolls, and archaeology all put together can give a reasonable picture (although all the sources need to be treated with care – many villages were abandoned after the Black Death because not because everyone died but because the survivors moved to better land). So we know Black Death mortality ran between a quarter and a third.

    In the Americas, there are similar problems, but we can recover quite a bit.
14. faustusnotes Says:

    
    January 26, 2020 at 7:28 pm

    J-D, I don’t know if the populations were diverse or out of contact because demographic data from 1492 is shit but I think we can all agree there is a general sense that this was the situation then. Do you really need to be this pedantic? I’m not justified in assuming it was spread by only Europeans but a) I don’t have the flight records from 1492, or any train data, and b) if the indigenous tribes weren’t in contact with each other but white people were spreading through the continent killing people and stealing their land we can maybe hazard a guess about how contact worked.

    I’m not trying to say that the information is new, I would hope it’s clear I’m trying to say that it has risen in the public consciousness over the past 20 years as the revisionists and genocide deniers have crawled out of the woodwork, led by arseholes like Windschuttle. For these people the story is very convenient, just as the typhus excuse is much loved of genocide deniers, and that’s why it seems to me that it has become more publicly disseminated recently[1]. I know the idea is older than Windschuttle, my argument is that I think the idea has been dragged out, dusted off and presented anew by public “intellectuals” and personalities as part of a revisionist movement. And I think that the original sources are potentially dubious. My point applies equally to Rise of the West: how good was epidemiology and demography in 1963 and how empirically valid are claims about populations in the 15th century? What you and Peter T are saying may seem theoretically reasonable but what is the empirical evidence?

    [This is not a loaded question btw. If you don’t have empirical evidence for a claim about demography you simply shouldn’t make that claim. If someone has presented empirical evidence that disputes your claim, or some other research – as I did above – then the onus is on you to find some demographic or empirical data that backs up what you think is so obvious. And I suspect McNeil’s contribution on this was weak]

    Regarding your specific point about how epidemics can lead to changes in immunity through the influence of genetic variation, how dangerous does a disease have to be before it has an evolutionary effect on a population? For example measles has a CFr of 0.2%, if it were 10x as dangerous in a naive population it would kill 2% of the population, which would not be enough to induce any evolutionary pressure. Peter T says (without empirical evidence I suspect) that measles was brutal in the colonies, but even if measles were 10x as dangerous it would only kill 2% of the population, hardly enough to cause wholesale evolutionary shifts that would make the whole population less vulnerable. Smallpox is a possibility, but if smallpox is even marginally more dangerous in naive populations than in Europeans it would wipe out the whole population – and the article I linked to above identifies only a total 50% reduction in population from all causes (please engage with the findings of that article if you want to pursue this line of thinking). I found another article in Scientific Reports with hideous analysis which reports mortality rates from measles in “virgin soil” populations in the Amazon of between 0.2% and 83%, but it’s super dodgy and the population data is “an estimate from before contact”, so largely this is epidemiologically useless. I really am having difficulty finding any empirical support for the claim that isn’t undermined by the lack of demographic data.

    Also I should point out that this same argument about evolutionary adaptation should mean that native wildlife are no longer vulnerable to cats. Yet the idea still passes around comfortably as standard received wisdom in Australia that native wildlife remain uniquely vulnerable to cats. I think it’s interesting that this argument works in one direction when it conveniently helps to exonerate white people from responsibility for genocide, and yet works exactly the other way when it gives white farmers license to be cruel to a typically feminized animal. I think arguments from genetics serve as just-so stories to defend whatever we want to believe – see e.g. evolutionary psychology – and we need to be more careful about checking the evidence behind these arguments.

    [I also suspect this is true about many of the “biological” arguments for why Aboriginal people are vulnerable to alcohol, because biological arguments conveniently enable us to avoid talking about dispossession, genocide, stolen generations[2], unemployment, poverty, overcrowding and abuse, all of which contribute to vulnerability to alcoholism]

    —
    fn1: As an example of this kind of thing in action, consider Jared Diamond’s description of the collapse of society on Easter Island, which is heavily disputed by Easter Islanders and largely ignores the role of colonialism on the island’s development.
    fn2: I hope you can recall the vicious and sustained campaign against Sir Ronald Wilson after he released the Bringing them Home report and the desperate efforts to discredit every part of the work on stolen generations, including the deplorable way certain conservatives behaved in 2007 during the apology. You should never doubt the strength and ferocity of the denialist campaign that was unleashed in the 1990s, and the willingness of its main activists to trample on any aspect of history, science, sociology or common decency in pursuit of their aims.
15. Peter Thomson Says:

    
    January 27, 2020 at 6:27 am

    Faustus – you are looking for the kind of evidence we have today. As you note, it does not exist. But other kinds do, and there are people who can piece together a picture using the different approaches to cross-reference each other. I instanced the many kinds brought to bear on mortality estimates for the Black Death.

    You are right about the deniers, but this kind of research is not driven by them. And it has a salutory lesson for us – once a disease escapes into a non-immune population it can, unless contained very quickly, lead to very high rates of mortality indeed.
16. Peter T Says:

    
    January 27, 2020 at 12:11 pm

    Incidentally, the Spanish flu killed around a fifth of Samoans. Part due to lack of medical facilities and negligent administration, but also lack of general flu immunity, I would guess.
17. J-D Says:

    
    January 27, 2020 at 2:41 pm

    J-D, I don’t know if the populations were diverse or out of contact because demographic data from 1492 is shit but I think we can all agree there is a general sense that this was the situation then.

    I do not know that there is a general sense that this was the situation then, and if there is such a general sense I don’t know that it is well-founded.

    This is not a loaded question btw. If you don’t have empirical evidence for a claim about demography you simply shouldn’t make that claim.

    That’s fair enough, as far as it goes. I don’t have information to make strong claims about demographic history, so I’m not making any. Insofar as your position is ‘We should be cautious about accepting any claims about the extent of the demographic impact of epidemic diseases introduced by the Columbian interchange’, I agree. I get the impression that you’re making some stronger claims than that, and I’m questioning the basis for them.

    Regarding your specific point about how epidemics can lead to changes in immunity through the influence of genetic variation, how dangerous does a disease have to be before it has an evolutionary effect on a population?

    By default I assume that anything which kills individuals in a way which is not random in relation to their genotype has some evolutionary effect. If there’s no genetic variation which affects chances of surviving measles, then there’s no mechanism by which it can have an evolutionary impact, but if there is then there is.

    For example measles has a CFr of 0.2%, if it were 10x as dangerous in a naive population it would kill 2% of the population, which would not be enough to induce any evolutionary pressure.

    Wouldn’t it? I don’t know what the basis for that conclusion is.

    Also I should point out that this same argument about evolutionary adaptation should mean that native wildlife are no longer vulnerable to cats.

    It points only to the conclusion that they are probably less vulnerable to cats than they used to be, but even that only to the extent that the cats have not also been under selection pressure to become better hunters of native wildlife.

    Yet the idea still passes around comfortably as standard received wisdom in Australia that native wildlife remain uniquely vulnerable to cats.

    It may be standard received wisdom, but even if it is that doesn’t obligate me to accept or defend it.

    I think arguments from genetics serve as just-so stories to defend whatever we want to believe – see e.g. evolutionary psychology – and we need to be more careful about checking the evidence behind these arguments.

    If your position is that we should be cautious about accepting biological explanations of anthropological data, I agree, but not if your position is that we should by default reject biological explanations of anthropological data.
18. faustusnotes Says:

    
    January 27, 2020 at 6:42 pm

    Peter T, again it seems your speculation is out of whack with the empirical data. Apparently Spanish flu had a CFR of 10-20%, and many areas globally saw death rates at this level (at least according to the wikipedia entry). Assuming that the population estimates for Samoa were accurate (unlikely) then the mortality rate is consistent with the CFR of Spanish influenza unleashed in a tightly confined setting with poor management of the disease and a bad health system. (The wikipedia entry says 90% of people were infected, so the CFR is consistent).

    Let us consider the plague as another example. Plague hit Europe in the 14th century and caused repeated waves of epidemics until the 16th century. It is estimated to have killed as much as 20% of the world population at the time (again, this is from Wikipedia), back when Europe was “virgin soil” for plague. Of course we don’t have good population estimates at that time but for example this study (pdf) reports on an analysis of Dowry Books and estimates a 20% fatality rate among young women in Florence during the century of peak epidemics. The case fatality rate for plague now is 60%, so if it was worse back then the 20% fatality rate would be consistent with perhaps 30% of the women of the time being infected. But you would think that if your theory of virgin soil was true, then by now the CFR for plague – after 800 years of adaptation – would be much lower than it was then. Yet the studies don’t bear that out. It probably wasn’t any worse then than it is now. I think it’s safe to say that if these diseases retain the same mortality rate after 800 years of adaptation then the theory might be a little weak.

    J-D, the basis for my conclusion that a disease with a 2% CFR can’t exert evolutionary pressure is that it doesn’t kill enough people to change the population. If it had a 90% CFR in 1% of the population and a 1% CFR in the other 99% of the population, sure it would remove that 1% of the population that were evolutionarily vulnerable to it (if it could infect the entire population) but then it’s CFR would go from 1.9% to 1%. But if it only affected half of the population randomly, it wouldn’t kill enough of that vulnerable 1% to make any difference to the population distribution of vulnerable genes, and so the CFR wouldn’t change much. A disease has to have a very large mortality rate to significantly affect population genetics, I would expect (I am not an expert on population genetics, this is just my guess). In the case of plague, for example, that 60% CFR could be 30% in half the population and 90% in the other half. In that case, the vulnerable half would be extinct after a generation and you would expect the CFR in the following generation to be 39%. That is an evolutionary influence, a selection pressure. But you won’t see that selection pressure with a low-mortality disease like influenza or measles.

    A far more valid explanation for the high mortality rates in new diseases is a) we don’t know how to treat them and b) they occurred mostly at a time when treatments were not available. This is important, as I say, because this misconception about how diseases work enables people like Keith Windschuttle to claim that it was disease, not war, that killed indigenous people, and that white settlers weren’t to blame (this is an explicit argument he made in his first volume). That position has consequences for indigenous people’s struggle, and we need to be aware of it and not promote it if it is actually, clearly wrong!
19. Paul Says:

    
    January 27, 2020 at 8:32 pm

    “A disease has to have a very large mortality rate to significantly affect population genetics, I would expect (I am not an expert on population genetics, this is just my guess).”
    Doesn’t the relationship between malaria and sickle cell anemia (SCA) suggest otherwise?

    Per your figures, malaria has a CFR of 0.45% in Africa, but sickle cell anemia is linked to it as a genetically useful adaption.

    NOTE: I’m unsure of the status of the evolutionary link (e.g. if anyone is suggesting the SCA prevelance is linked to the relative level of malaria), though the usefulness of the SCA variation in resisting malaria appears to be documented and even understood.

    If SCA and malaria is an example, then potentially time frames for the exposure may also factor into the evolutionary driver(s).
20. faustusnotes Says:

    
    January 27, 2020 at 10:55 pm

    Paul I think malaria and sickle-cell anaemia are different. In this case sickle-cell anaemia persists in the population because it confers immunity to malaria, so something that over a human evolutionary timeframe should be bred out actually has a balancing positive effect that protects it. Also I think the malaria/human relationship has been around for millenia, probably as long as humans, whereas a lot of other diseases (like plague, influenza, swine flu) post-date the development of agriculture (since they’re zoonotic) and thus have much smaller evolutionary timeframes. The argument being given here is that plague was novel to western humans 800 years ago; smallpox was novel to new world humans 500 years ago; and they then develop some evolutionary immunity to it in rapidly short timeframes that mean subsequent waves of the disease occurring in the framework of human history see noticeably different mortality rates.

    My suspicion is that for humans to evolve immunity to something like influenza (rather than inheriting it briefly from our mothers) we need a lot longer than a few thousand years, if at all. Smallpox, for example, may have only existed in humans for 2500 years, whereas there is evidence of malaria parasites existing 30 million years ago (for some reason Noah thought putting two mosquitoes on the ark was a good idea!) Maybe there’s a relationship between the CFR of a disease and the evolutionary timeframe required to develop good immunity in the population, but my suspicion is it’s very, very long!
21. faustusnotes Says:

    
    January 27, 2020 at 10:55 pm

    Sorry I should say “the case of malaria and sickle-cell anaemia are different to the case of influenza immunity”.
22. J-D Says:

    
    January 28, 2020 at 9:51 am

    A disease has to have a very large mortality rate to significantly affect population genetics, I would expect (I am not an expert on population genetics, this is just my guess).

    I’m not an expert on population genetics, either, so I’m not going to guess, but I’m not sure your guess is correct. How large does the impact of variation in tooth size need to be to explain the observed evolutionary trend to smaller human teeth?
23. faustusnotes Says:

    
    January 28, 2020 at 1:46 pm

    That’s a process that happened over millions of years. The developments being described here seem to be things that are expected to happen over a couple of hundred. This not very satisfactory article gives the age of some common infectious diseases and the development of resistance, and suggests that diseases have to have been around a very long time before selection can begin to occur – for example it says smallpox probably existed in Africa 10,000 or more years ago which might explain lower mortality rates in Africans. It also suggests that the study of natural selection and infectious diseases is still very much in its infancy and there are many unanswered questions.
24. Peter Thomson Says:

    
    January 28, 2020 at 2:52 pm

    From my reading in genetics (not an expert, but well-read in lay terms), 2% additional mortality, applied selectively, would be a very big deal indeed.

    Faustus – that reactionary idiots use some fact to beat the left does not necessarily make it false. The evidence that disease had a devastating effect on Amerindian populations is not really in dispute, nor that diseases ran ahead of white contact. Archaeological and scientific work has tended to raise upwards the estimates of the population of the Americas, and surveys show large-scale abandonment of agricultural lands, reversion to forest and to hunter-gatherer lifestyles even in areas where white contact was long delayed.
25. J-D Says:

    
    January 28, 2020 at 6:00 pm

    That’s a process that happened over millions of years.

    It’s detectable over a much shorter time scale.

    It also suggests that the study of natural selection and infectious diseases is still very much in its infancy and there are many unanswered questions.

    Either the knowledge base is sufficient to draw conclusions or it isn’t. If it’s insufficient to support the conclusions you’re objecting to, it’s also insufficient to support your conclusions.
26. faustusnotes Says:

    
    January 28, 2020 at 7:03 pm

    Peter T, the plague has been around for 800 years with 60% mortality but it hasn’t managed to exert any evolutionary pressure on the human population. Why do you think that 2% should matter?

    Also, regarding “that reactionary idiots use some fact to beat the left does not necessarily make it false.”: Windschuttle explicitly (and infamously) recalculated the number of deaths due to murder in colonial Tasmania to ensure that he could argue the Aborigines there were primarily killed by demographic factors. It is often the case that facts in history are subject to dispute, recorded by the victors, and misused by their defenders. So it very much may be the case that these “facts” are false or highly disputed. In fact I discovered there’s a whole book on this, called Numbers from Nowhere, that is quite eye-watering in some of its claims. This topic has seized my attention so I think I’m going to write a separate post on it. Stay tuned!

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