if you want to debate your arguments even assuming your premise, the above simply doesn't hold. — boethius

Actually, please just ignore the last two paragraphs of my last post. I don't really want to discuss that. I just wanted to explain some of the reasons I thought it was important that we don't avoid the possibility of an overlap. It really makes no difference at all if I'm wrong about all of them (presuming we're not deciding what's right on the basis of what it would be convenient to be right).

I don't want to hold two discussions at once (one is hard enough to keep up with). There's enough to discuss just on whether there is an overlap without adding whether it would be beneficial to publicise that fact (a completely unrelated question).

I gave lot's of reasons why there is no such subgroup of "weakest heart" as lot's of factors affecting real death from heart disease are in the future and therefore Covid cannot select for. — boethius

No, you gave a small number of minor factors without any citations to back them up and nothing to counter the cited evidence I provided of the major factors which do overlap.

My whole position is based on a well known statistical fact that as selection from a group becomes a small, the chance of colliding with some other small selector is small — boethius

Yes, and you've yet to demonstrate, with evidence, that the selection is small (relative to the group {at most risk}, nor that there is 'some other' selector rather than exactly the same one.

A loan doesn't help a doctor today treat a Covid patient, only real material and human resources (which cannot come from the future) — boethius

It's a start. A start which is more likely to be made if people are not overduely concerned about preserving resources for some future apocalypse.

Government have already implemented rationing successfully, even some chains voluntarily implemented rationing. — boethius

So your complaint about the US government in this regard was about what?

there's no way to re-assign resources from the future to the present. — boethius

There is. Loans, postponing leave, postponing retirement, postponing investment plans. There's all sorts of ways of borrowing from the future.

In the US this would be socialism and "a republican" administration doesn't want to set precedents that socialism can help on some issues — boethius

Right. So you're wrong when you say that governments can deal with these problems through rationing then aren't you? Governments are elected by (Influential sectors of) populations, populations which at the moment are increasingly right wing, so government can't help in the way you suggest. It's no good planning a response strategy based on a pipe dream of what we'd like the world to be. "The first thing we need to do invent a time machine and ensure we get a more socialist government elected", is that your plan?

Here's David Spiegelhalter explaining what he means by those figures. He's very good at explaining these things (it is, afterall his job).

So, if the factors which cause fatality from Covid-19 are largely different to the factors which cause fatality in general, how do you explain the fact that fatality risk from Covid-19 tracks fatality risk in general almost exactly?

Why would a 70 year old face exactly the same increase in risk from Covid-19, compared to a 19 year old, that they do from all diseases combined without a majority of significant overlapping factors?

Say mortality from Covid-19 is determined largely by a factor-A, and mortality from heart disease is largely determined by unrelated factor-B. Your risk would be related to the prevelance of the related factor. Unless both of these factors, despite being unrelated, coincidentally increased at almost exactly the same rate with age, then the match in increase of risk with age would have to be a massive coincidence.

The fact that the risk from Covid-19 tracks almost exactly the risk in general shows that the factors causing risk in Covid-19 are likely to be the same as the ones causing risk from disease in general.

The graph I just posted (if true or close to true) demonstrates the basic problem, as it would mean (if everyone got the disease) about double total deaths in the year — boethius

No it doesn't because it is comparing the estimated risk from Covid-19 compared to the normal risk for a year taken ftom years in which Covid-19 was absent. It doesn't tell us anything about the relative risk from other diseases in a year where Covid-19 is present.

Hardly any ancient farmers died of cancer. It's not because they were super-healthy, it's mostly because they died of something else first. It's the same with these figures. The risks for a year in which Covid-19 is not present to kill you first are not going to be the same as for a year in which it is.

If you really want me to go into the calculations that explain my position, I can do so. — boethius

Yes, that's what I've been repeatedly asking you to do.

The number of people recorded as having died 'of' a particular condition is heavily dependent on the manner in which the death certificate is recorded and examined in data harvesting. The CDC figures for ILI from 17-18 is recorded in the same way as Covid-19 (listed as a contributory factor on the death certificate), so it should be comparable, but we've no idea how doctors and coroners were instructed to list flu in 1958, so the figures are not accurately comparable.

Death certificates are notoriously difficult to extract good data from, especially across medical paradigm changes.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4808686/

Just in case anyone else has jumped to the conclusion that because I mentioned the statistical implications of overlap in mortality cohorts I'm obviously either a heartless fascist or duped by one...

The reasons I think overlap in mortality cohorts is important are;

1. High overlap undermines certain arguments against social distancing measures because there should be little net excess in treatment requirement, focusing the main problem even more in the height of the spike of cases. Without overlap there is an argument that flattening the curve will not help because it pulls staff from other vulnerable cases in the long term so providing no net gain. In other words, with overlap we only need to re-assign resources (which everyone agrees is doable), without overlap we need to produce a net increase in resources (which many think is not doable, so why bother >> herd immunity bullshit).

2. Perpetuating the idea of no overlap in order to procure these additional resources (and likewise avoid providing an excuse to those who don't want to pay for them) may well work in the short-term, but a) it's hardly a long-term strategy for procuring more investment in health care, and b) it undermines the credibility of socialist arguments if the threat does not then materialise. We shouldn't pin arguments about investment in healthcare to the severity of rare pandemics when there are perfectly sound arguments for it which are already demonstrable.

3. Using fear to bring about policy change is a dangerous strategy as the very institutions and cultural practices which are necessary to make it a success do not in themselves act as filters for the sensibleness, humanity or practicality of the policy being thus advocated. Fear can be useful politically, but it does not have a good long-term track record of maintaining positive change.

4. The extent and nature of any short-term change in demand on healthcare systems is crucially important to the management of those systems. We can bemoan the shortfall in net funding all we like, but somone still has to make ten bandages fix twelve broken arms, so to speak. They need to know what the future calls on their insufficient funds are likely to be. This is less relevant to public discussion, but public mood does filter into policymaker's discussions, they're only people after all.

5. We will have to come out of lockdown soon (partially) and continued promotion of the idea that Covid-19 is some random reaper stalking the land takes resources away from those who really need them as the hysterical-selfish (by far the largest population group) panic-buy themselves their ppe/food parcel combo (Disney-themed, Bluetooth-enabled version, only £9.99 on Amazon), while doctors make do with paper towels and some sellotape.

Edit - I forgot to add that I just don't like it if something seems wrong, so even if none of the above were true I'd still be arguing about the statistical implications of an overlap in mortality cohorts just because I think there is one, and I'd rather hope to be discussing things with people intelligent enough to know the difference between a fact which is unhelpful and one which is wrong.

This data supports my point not yours. Hypertension, diabetes, etc. are very large risk groups from which my analysis follows. — boethius

Just repeating that your analysis is right doesn't make it right. Them being large risk groups does not in itself mean that they are not graduated along the same factors as constituted membership.

If risk groups are large, then the "people who we would expect to die this year from the existing pattern" are unlikely to intersect "people who actually die from Covid". — boethius

There is no reason at all why this follows from the risk groups being large. they would also have to be unsorted (by the same factors) but you've not shown any evidence that this is the case.

Furthermore, you've simply ignored the other reasons we shouldn't expect Covid deaths to be displacing near-future-otherwise-deaths even if there was unknown "weakest heart" kind of groups within these groups, such as diabetes, hypertension etc. such as the simple fact we're early in the outbreak. — boethius

No, the fact that the group membership is dynamic only affects the risk estimates if the group is changing (growing or shrinking). The risk group for heart disease, diabetes, cancer, etc is not growing or shrinking. It is remaining roughly the same size. The rate at which people's risk factors reach the threshold to cause them to join it is roughly the same as the rate at which people leave it (whether by death of by getting better). If more people leave it by death then the group will get smaller by exactly that number. the fact that some people also leave by getting better doesn't make any difference to that effect. again, all these factors are the same, and the articles I linked show this. Even if you focus on the people who leave the group by getting better, they are still more likely to be the people with lower scores in the key factor than those with higher scores. Exactly the same factors determining likelihood of fatality from Covid-19.

I've yet to see you present a single piece of evidence showing that factors other then those we mentioned (hypertension, diabetes, suppressed immune system, failing supporting organs, lung damage...) are not the main factors determining fatalities from either the covid-19 group, or the {heart disease, cancer, lung condition} group.

It's pretty simple - so long as they are the main factors determining fatality in both groups, then covid-19 fatalities will be overwhelmingly drawn from the same pool as heart disease, cancer and lung condition fatalities.

So rather than just repeat that you're right, again, or point out that other obscure factors do come into play, again... why don't you link to some scientific papers showing that the factors listed are not the main factors determining fatality in either group. Otherwise I've nothing further to say on the matter.

(Oh and if you try and play the "you've been duped by ideology whereas I remain coldly rational and unaffected by such weaknesses" card again I will not respond - let's presume we're all intelligent, relatively equal people until proven otherwise shall we?)

First, I've already explained why those factors can't be the same as some of those factors are in the future. So I guess deal with those first. — boethius

I'm just repeating myself, and so are you, so this is getting pointless. You're pointing out that the factors do not entirely overlap. I'm saying that they oveap in the vast majority. If all you're going to do is provide instances where they don't overlap we're not going to get anywhere. I'm not arguing that there are no such instances.

Here's some basic resources on risk factors for heart disease (as an example).

https://www.who.int/cardiovascular_diseases/en/cvd_atlas_03_risk_factors.pdf

https://www.nhs.uk/conditions/coronary-heart-disease/causes/

Here's the preliminary findings on risk factors for Covid-19 mortality.

https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(20)30566-3/fulltext

https://www.bmj.com/content/368/bmj.m1198

Note the repeat of hypertension, CVD, diabetes...

Note the complete lack in either case of mention of locality, blood type, luck, or some as yet unidentified genetic factor or in fact any of your obscure factors.

I mention otherwise benign genetic differences (that benign differences can have a significant outcome difference given some new threat — boethius

You keep talking in vague generalities and obscure factors. To support your position you have to demonstrate that the vast majority of factors defining the most vulnerable people in the group suffering from heart disease, lung conditions, cancer etc are not the same as the factors defining the most vulnerable people in the group of Covid-19 sufferers.

Not just one or two areas in which they might differ.

So common factors like weakness of the heart, suppressed immune system, overworked supporting organs, stress, comorbid infections, lack of exercise.... All these common factors.... You've got to come up with a list of uncommon factors which is bigger and has a net larger influence on fatality in each group.

The last official figures show that there were 6000 deaths registered above average. That is around 50% above average so hard to ignore without a damn good explanation. — I like sushi

Have you seen people ignoring it? Last time I looked the world was practically hysterical about it. There's certainly a considerable disagreement as to how best to proceed, but I think everybody's way beyond ignoring it.

Other factors can easily dominate in selecting for death within the heart disease group. — boethius

What are these factors then (presumably ones which don't also overlap with factors making death from Covid-19 more likely)?

Furthermore, a big determining factor for surviving a heart attack is time and place, and this is a completely independent variable to Covid — boethius

Really? In what way? Presumably proximity to medical services is the key variable in time and place (those more remote will have more difficulty). How is that different with Covid-19?

people may improve or deteriorate their lifestyle moving from this "weakest" category to "ok" or vice versa, or a really stressful life event has an acute impact on heart disease likelihood; failing to seek timely treatment etc. — boethius

Again, how do these categories differ from those which relate to vulnerability to Covid-19 fatality? Stress, for example, suppresses immune response.

there's simply no reason to assume deaths from Covid overlap with some unknown "particularly unhealthy" sub-group of heart disease. — boethius

Firstly, yes there is a reason. Those most likely to die in the "heart disease" group are those with the weakest hearts (for various reasons), those are the same people who, within that group, are more likely to die from Covid-19. It is the inability of the heart to support recovery which causes the fatality, not some dice-rolling random factor. The exact same factor.

Secondly, even if the studies relating heart disease to Covid-19 deaths turned out to be wrong about the mechanism, there are still no studies showing the opposite (as you are claiming) a lack of overlap in mechanism.

As I said, if you're going to spread hysteria, you'd better have damn good evidence backing it up, not a bit of guesswork and a lack of contrary evidence.

An example, it seems blood type O is particularly resistant to Covid, but blood type O does not provide a similar resistance to smoking — boethius

This is trivial compared to the disproportionate risk having heart disease, lung conditions or undergoing treatment for cancer has on your risk from dying of Covid-19. Those are overwhelmingly the main risk factors. They are also overwhelmingly the main risk factors for death in general. Minor variations in genetic make up (which do not also affect things like infection, heart disease and cancer) are just that... Minor.

No it can't, if you're trying to support the idea that Covid kills the "particularly unhealthy". Lot's of "particularly unhealthy" simply don't get the disease, so there will remain lot's of these "particularly unhealthy" around since they didn't get infected. — boethius

I'm not suggesting none of the "particularly unhealthy" will remain. Only that they constitue both the cohort from which Covid-19 draws most of its fatalities and also the group from which the general death rate draws most of it's fatalities.

Being the same group means that if one draw reduces the numbers, the other will have proportionately fewer to draw from.

I'm saying there's no reason to assume the variation of death and survival within a risk group is due to being "particularly unhealthy" within that group. It could be some other mechanism such as otherwise benign genetic differences, or then simply random variation such as where exactly the virus begins replicating in the body, that then dominates chances of death within a risk group. — boethius

Well then support that theory with evidence from the literature. Otherwise it's just idle speculation and you're using it to fuel serious fear and panic so it had better be damn good evidence.

For this to be true, the "less healthy members" within a risk group need to somehow be far more likely to get infected to begin with. — boethius

No they don't, because if everyone is equally likely to be infected then the liklihood of infection can be removed from the equation. It's only relevant if it biases fatality in the opposite direction. We're looking at whether fatalities are going to be significantly disproportionately drawn from certain groups. If 10% of all groups become infected, then we're dealing with 10% of the healthy cohort vs 10% of the least healthy cohort.

It could be random genetic differences that make a person in a risk group, such as smoking, particularly at risk of Covid. — boethius

Unless you're suggesting that there's some gene specific to the defense against Covid-19, then the only genetic component which might be relevant is one which affects the immune system in general. Such as defect would put you in the cohort from which the 300,000 yearly deaths are drawn.

The random mechanism is that we don't know who within a risk group is actually going to die this year, — boethius

Yes we do. It will (disproportionately) be the least healthy. Same as those most likely to die from Covid-19.

It might be different in a country whose disease-related deaths were mostly infections (like some developing countries) but not in the Western world. Our deaths are drawn overwhelmingly from heart disease and cancer. The exact same groups from which Covid-19 is drawing most of it's fatalities (with cancers being mostly the immune suppressing effects of treatment).

Nothing I have said contradicts this. — boethius

Then where is the random mechanism? If you agree that it is failure of the immune response and supporting organs which leads to death, then it directly follows that those with the weakest immune systems and supporting organs will almost exclusively be the group from which fatalities will be drawn.

If you want to claim fatalities are drawn randomly from that group you need to describe the random mechanisms, so far all we have agreed on are non-random mechanisms directly related to health.

No, there's no causal mechanism that will cause significant overlap, unless by significant you mean measurable. — boethius

Covid-19 kills people either by the lungs filling with fluid as a result of a failure of the immune system (sometimes from comorbid bacterial infection) or by exacerbating the effects of other conditions, particularly heart disease. Every single one of those mechanisms relies on an underlying health problem. If you know of some way Covid-19 applies a random element to the selection of fatalities, I'd be interested to hear it. As it stands, if you lined up 1000 people in order of healthiness and gave them all Covid-19, the one who will die will be drawn from the least healthy end. Likewise if you lined up all 70 million people in the country in order of healthiness, the 300,000 who are going to die this year (from disease) will be drawn from the least healthy end. It's the same cohort.

I don't know how else to explain this. There are 300,000 people who are so ill that they're going to die this year. You're suggesting that when these people get a Covid-19 infection, they're not significantly more likely to die from it then anyone else, that the deaths won't be drawn with any significant bias from this group.

Being in an at-risk group increases your risk of dying if you get Covid, but the progression of Covid, in itself, does not significantly alter the nature of those risk groups going forward, such as culling the people that would actually die soon — boethius

Of course it significantly alters the nature of the risk groups. So far 98% of Covid-19 deaths are from these risk groups, so if Covid-19 kills 20,000 people, then these risk groups will be 19,600 people smaller than they were beforehand. They are not like an exclusive club, they don't have a waiting list. If 19,600 people suddenly get removed from these groups, there's not a reserve cohort waiting to take their place. The 300,000 deaths are also drawn mainly from these cohorts. Again 300,000 is not a quota to be filled. If Death finds fewer people in his preferred selection group than normal he's not going to go looking elsewhere to bump up the numbers.

Smoking, obesity, being old, are very large groups. Covid killing some people in those groups is just as random as other causal mechanisms that make these risk groups exist. — boethius

No it isn't. Even within a risk group, the least healthy members of that risk group are more likely to die than the most healthy. There's no dice in our bodies that a virus gets to roll to see if it's going to kill us or not. It's a direct and unmediated consequence of the response of the immune system and the function of supporting organs. There's no roulette wheel involved.

you can't be madly in love with your girl if you think your girl doesn't exist. — David Mo

Ahh yes. The search for external social group validation for one's beliefs. You know that's a fairly modern phenomena? It's not really seen in hunter-gatherer communities (but then there has been much less work done on them, so it might be found one day).

It's what (generally) drives this desperate insistance that there are objective truths. The full assertion goes "There are external, objective truths in the world (oh, and the ones that there are happen to be all the ones I already think)"

You see this in everything from scientific paradigms, through politics to ethics. The quest for some external social validation to shore up an otherwise crippling lack of confidence in one's approach.

" We can determine truth from logic" - means 'I'm not getting the proof I need empirically, so I'll add a few laws in and make my assertion sound more authoritative'

"There are some ethical positions which are beyond debate" - means 'a the ethical positions I don't agree with would be easier to dismiss if I didn't have to discuss them'.

"We all agree on certain truths" - means 'We all agree (with me) on certain truths'.

It's (unsurprisingly) more common among intellectuals who didn't receive the validation they wanted from their peer group for their success relative to those with physical skills.

Now - get off my couch and pay the receptionist on the way out.

Iceland has, to my knowledge, done the most extensive testing so far. Their (preliminary) results are here

The other respected dataset is Estonia which is here, but you'll have to translate the page.

All methods of obtaining truth refer to propositions based on intersubjectivity, experience and prediction. That goes for your dog and for an electron. This is what we mean with "Give me a proof of this". — David Mo

Yes, I'll certainly grant that they have that very broad range of factors in common. But not all cases have all three. A mathematical truth has nothing of prediction or experience, a 'true' note in music has only inter-subjectivity and experience, the true statement of past events has nothing but inter-subjectivity alone.

Then comes the discussion about whether the truths thus obtained are objective or not. — David Mo

Why? What does this add to the methods we already have? And how could we possibly proceed in such a discussion when the truth of the solution can only be established by inter-subjectivity, experience and prediction?

Introducing a new pattern that has no causal mechanism to significantly overlap (and thus displace) an existing pattern simply results in more deaths and no first-order reason to believe deaths will be lower when that pattern goes away. — boethius

But it's not a pattern which has no causal mechanism to significantly overlap an existing pattern. Why do you think the government has sent out specific advice to vulnerable people? What biological mechanism do you think takes place to account for variation in disease course if not the ability of the immune system to respond? Viral load is certainly one factor, but it's unsure at this stage whether that's even a significant factor (one study says it could be, two other say it isn't, but those have yet to be peer reviewed).

So as things stand we're left with immune system response as being the only mechanism that has been reliably demonstrated to account for the variability in outcome. Meaning that literally everyone who experiences a poor outcome does so on account of a compromised immune response (except as I said, if the Lancet paper is right then very hight loads such as healthcare professionals are exposed to could be a factor too, but not for the general population).

So how do immune responses become compromised other than by underlying health conditions?

Likewise, most people at risk of respiratory illness will also not die this year nor people suffering from heart disease. — boethius

No, and most people who get Covid-19 won't die this year either. That's not the point. The point is that of those people who will die, a disproportionate amount will be drawn from that small group of people who were going to die from respiratory illness or heart disease. We're talking about quite small proportions in either case, so it's no good saying that only a very small proportion of those with underlying health conditions were going to die this year anyway. We know with great precision how many of those people were going to die this year anyway, its about 300,000 (the death rate minus deaths from accidents). So until the death rate from Covid-19 exceeds 300,000 you can't possibly say that the victims were not going to die anyway, simply on the basis of the numbers, you additionally need data on the overlap - or you need to wait for deaths occurring over a longer timescale - say a year, or you need a plausible mechanism of fatality which does no coincide with underlying health conditions.

People will continue to die of hear attacks for instance; there's no reason that Covid is killing people who really would die of a heart attack this year compared to people simply at risk of dying of a heart attack — boethius

Again, not to labour the point, but there absolutely is such a reason. People who are going to die from heart disease this year will disproportionately be in worse general health (specifically cardiovascular health) than those (from the same cohort) who were going to last more than a year. Death does not harvest randomly. Those who were ill enough to be likely to die this year from heart disease are more likely to die from Covid-19. That is why we see a disproportionate number of deaths in these categories.

maybe other second-order effects increase causal death mechanism, such as lung injury. — boethius

Again, not comparing like with like. If you're including (in your risk analysis) for Covid-19 potentially related deaths, then when comparing it to risks we know already, you have to do the same. Many illnesses have related tissue damage which causes morbidity later on, we don't include it in the death statistics for that condition - so why would we change our statistical approach for this particular condition?

Covid-19 may well be with us for some years, and if not this, then the next one. We have to manage it (and more importantly learn to cope with it psychologically) in a sustainable and consistent manner. I understand the impetus, but artificially making it sound more terrifying than it already is does not get people to act in the rational manner needed at times like these, nor is it healthy for the population in the long-run (not that the mental health of the population in the long run isn't already a lost cause - one might as well be holding back floodwater with a sieve)

Yes, perception is a simple criterion. It's more or less useful in everyday life. But it is useless in propositions about electrons or force fields. This is where the problem of true propositions begins.

If you have thought that defining truth is simple, you are wrong. — David Mo

But I wasn't talking about using perceptions to define 'truth'. I was talking about using perception to distinguish 'true dog' from 'false dog'. There is no general case which covers 'true x' and 'false x'.

When it comes to electrons, physicists are not even thinking in terms anything like the dog example. They're thinking in terms of fitting data to a model with predictive power (or elegance, or simplicity...). Here it's not 'true dog=pat it - false dog=run away'. It's 'fits the model=publish - doesn't fit the model=revise the model' (to put it very simply). In neither case does the scientist or the would-be dog patter need a general definition of truth to hold or perform either of those two algorithms. Experience is sufficient.

I think "comorbidities" has given a lot of people on the internet the impression that most people who die from Covid are essentially on deaths doorstep and the virus was a, perhaps even in their minds a merciful, coup de grace. However, these underlying conditions that increase the probability of death are very large, fairly banal groups; people with heart disease, diabetics and cancer survivors that have relatively long life expectancies. Large groups where there's no reason to believe those that would die of some respiratory disease anyways, — boethius

500,000 people die every year - from which group do you think these deaths are drawn? If these groups do not form the ones who would have "died anyway", then from which group are the 500,000 people who do "die anyway" drawn? Are you suggesting that chance of death is essentially random and not related to underlying health conditions?

The statistical analysis of this general issue I've seen so far, is that getting the virus doubles your chances of death of the year compared to your risk group. — boethius

Where's this? Just on the face of it if this were true then we'd expect to see a doubling of the death rate in all age groups, yet we see absolutely no impact whatsoever in age groups below about 65 (decreasing in statistical significance of course, rather than a single cut-off point).

The rest of your post seems based on this so we'd better sort out what support you have for that assertion first.

it's rare to see more than one virus at a time. — frank

Can't find the exact article I remembered so I'll defer to your greater expertise and presume I either remembered it wrong or misunderstood it in the first place. I had a brief look online and it is certainly common to be infected with more than one virus at a time, but the only similar figures to the ones I quoted were for HRV so that might be where I've gone wrong.

No idea what that means or how it counters anything I said? The figures give are for week ending April 3. Clearly there is a spike in deaths. — I like sushi

Yes, but people can't die twice. 10,000 people die every week, different proportions for different cohorts, but with elderly and those with underlying health conditions, the proportions are obviously higher. So if, rather than 10,000, 16,000 dies one week, that's 6,000 fewer people who can die next week (they're already dead). No-one's increased the entry to that cohort (the birth rate wasn't raised in advance 80 years ago), so the effect will be seen in the following week. More so by a year.

The chances of and 85+ person dying are about 1 in 6 annually. So in any given year, one in every six of that cohort are going to die. That's about 280,000. If 20,000 die from Covid-19, the other diseases aren't going to 'seek out' their usual number of victims, they haven't got a quota to fill. There are simply going to be fewer people in that cohort so the percentage of them dying of the same diseases is going to lead to smaller number. If a disease preferentially causes fatality in those with underlying health condition, then that is the cohort against which it's impact should be measured in this sense. Obviously that cohort is not going to be added to at an increased rate, but it is going to be removed from at an increased rate so there will be a much smaller pool for the remaining illnesses to draw their mortality from.

The figures for deaths (ALL deaths) are not ‘crude’. The deaths for last week ARE crude - meaning they are not official figures because it takes time to account for all deaths. — I like sushi

No, still not what I'm getting at. The cohort for whom the deaths in one week are related are not the cohort for whom the case numbers are given. Any in that cohort who are going to die are going to be reflected in the next fortnight's figures.

An extra 500 cases is a significant rise though. — I like sushi

Fair enough. It's pointless quibbling over what 'significant' means, so I won't.

Maybe you’re comparing April to Dec and Jan. That is faulty because the death toll during the winter months in the UK is always significantly higher — I like sushi

No it isn't faulty. The deaths are higher in winter because of flu. So, given that we now have a new flu-like illness (but one not yet clearly seasonal), comparing it to it's most similar condition is entirely appropriate, I think. No-one's saying there's no deaths being caused by Covid -19, the issue (for risk analysis) is how many compared to other diseases we've dealt with. The most obvious comparison if flu at it's worst. That's something we've dealt with before. 2000 deaths a week is not much different from flu at it's worst, so we can use that for response planning.

The death rate clearly spiked in the last reported week. I guess it could be argued that this is due to other causes but they’ve clearly marked respiratory problems and Covid. — I like sushi

So

1) A spike in the death rate is only a snapshot at a particular moment. The 6000 extra people who died last week are not now available to form the pool of people who will die next week. This would be irrelevant if Covid-19 did not preferentially target those with underlying problems, but it does.

2) 'crude' here doesn't mean estimated, it means that the actual people forming the deaths are not the same actual people forming the cases in the same week. So saying 'x deaths from y cases this week' is a crude figure. The x deaths came from the amount of cases there were last week (assuming it takes people a week to die).

3) 2000 cases from respiratory conditions is not far off normal. It's the amount of cases with underlying health problems being pushed over the edge that is the real problem here. The key thing there being that we don't know how many of them would have died anyway, nor will we until the year's figures are out.

Anecdotally, I look at respiratory viral panels all the time and it's rare to see more than one virus at a time. — frank

Interesting. I'll dig out the paper I got my figures from when I get home. I may have misunderstood it.

I don't want to step on your obviously far more qualified toes, but I think you missed a few (while we're making a list), please do correct me if I'm wrong.

(4) If you're using the death statistic to compare to like diseases, you cannot discount overlap. Most groups of people who die have an average of 2 viruses present at the time of death, sometimes as many as 5. Only one of these is going to be recorded as the cause, and right now, it's going to be Covid-19. The bias here will increase as the pandemic takes hold. About 10,000 people die every week (in the UK), an increasing proportion of these are going to have Covid-19 in their system at the time of death.

(5) Similar to (4), someone who dies of Covid-19 is not then available to form part of the pool of people who are going to die of something else. So this will affect net deaths, but also proportional death (when comparing causes).

(6) The peak of a curve and the extent both contribute to the total. We're presumably concerned both with the raw number of deaths and the rate of increase. I've seen a lot of reporting which confuses the two. A high rate of increase does not necessarily mean more deaths (it depends on duration), and likewise the other way around.

(7) The deaths reported are crude numbers so they don't represent the actual changes in death rate (they're lagged by a few day from the rate for actual cases). This means that the proportion of deaths to cases will artificially a bit low as the pandemic progresses, but likewise artificially a bit high as it subsides.

How can you say there is a dog if you don't have a criterion to decide what is a true dog from a false dog? — David Mo

If, when I pat it, my arm goes right through, it's probably a false dog.

But this is just tautology, as here 'false dog' just means 'one which my arm goes right through when I try to pat it'. We're just sorting things into classes and giving those classes labels - 'True Dogs', 'False Dogs' - according to some criteria of experience which seem to work for whatever we're trying to do with those classes at the time.

That's about what we do do, not what we ought do.

What ought we do? — Banno

I'm afraid psychology doesn't cover what we ought to do (despite the appearances to the contrary from some of the field's more nefarious representatives). So I don't think there's any fact of the matter about that question.

Personally, I think it's unavoidable and so there little different one ought to do other than carry on. It's possible to become more adaptable and less frightened of contrary (or absence of) information. That certainly reduces the backfire and continuous influence effect (respectively - hardening one's position in the face of contrary evidence, and seeking only confirmatory evidence - if you're not familiar with the colloquialisms).

But then, being adaptable becomes a paradigm in itself and you end up vacillating unnecessarily just because it fits your self-identity. You can't win. Just pick a good story to start with and be prepared to drop it in the face of overwhelming evidence to the contrary, but don't be too quick to drop it just because it's got a few cracks in it, everything has, and we need those stories to be quite robust and dependable. It's no good becoming a ruthlessly logical fact database at the expense of ones sanity.

I'm trying to figure out how you hurt your foot without accessing objective reality. Your perception of the table didn't cause an injury. — Cheshire

Of course it did. What is a nerve signal if not some form of perception?

If there was no objective reality* then we can't be wrong about anything — Cheshire

Why on earth not? I was wrong to kick the table leg because it hurt my foot. There need not be access to an objective reality to make that the case.

Your answer? — Banno

Physiological I'm afraid. Philosophers, scientists and forum posters all share the same primal fear of not being able to predict the outcome of their actions. Do do this they need a model (bayesian, of course) and seeing as the outputs of some models form the priors of others (Quinean Web of Belief stuff) the notion of having to change one small part of the Web becomes more distressing the more interconnected that node is. Leaving the contents of that node to an external source seems to make it more vulnerable to future change, so we avoid it. Re-enforcing those beliefs by seeking mutual approval for them is comforting, as is doing so by fitting them, post hoc, to facts others agree on.

The more frightening the potential consequences, the less uncertainty people will express about the consequences of certain courses of action, regardless of even their own assessment of certainty in less perilous states.

let's just refer questions about Covid-19 to the medics, not the philosophers. — Banno

And yet there's a 109 page thread about it, full of budding Nostrodamus's, exhibiting the seemingly universal human trait of defining what is 'true' by reference to a embedded narrative, rather than a reified ideal of a shared reality.

Yes, it is - that's part of the point. "...is true" is banal. It adds nothing to what has already been asserted. — Banno

Wow. That will come as shocking news to the millions of people who use it every day to add something to their assertions.

"It's true...I really do have a tattoo on my back";

"It's snowing?...Are you joking?", "No, It's true, It's snowing"

"You're lying to me, the documents aren't in the case!", "No, the documents are there, it's true, I swear!"

"He's an honest man, if he says he wasn't at the bank, it's true that he wasn't at the bank"

Are all those instances of 'is true' really adding nothing to what has already been asserted?

Or is tempering philosophical whimsy with reality something which applies only to some philosophical projects and not others?

Because truth and belief are connected. Sure, you can have a notion of "objective truth" that is completely divorced from whatever anyone thinks about the world. But by that same token, it'd be completely empty. If there is no way to establish truth, then judging things as true or false is pointless. — Echarmion

This is a point which is in danger of being lost in the weeds, so I wanted to re-raise it.

@Banno is (as he did last time we discussed this) trying to use the likelihood of a shared set of stimuli to for an argument about the meaning of a term.

Banno's 'thread' and my 'thread' seem likely to come from the same shared source. Without such a thing we couldn't even talk about the differences between our subjective versions, but the mere existence of such a thing does not constitue proof that the word 'truth' refers to that thing, nor even that it should.

No, I don't think I will. — unenlightened

That's pathetic. You make a simple assertion and you can't even back it up on request. This is what passes for philosophical discussion here, a series of bare assertions, spectacularly unsupported guesswork where science should be, a few rounds of cheerleading from the old boys club and shut down any argument you can't respond to with a cliched insinuation that you're opponent is so wrong it's not even worth your precious time showing them how. It's the same story in every other bloody thread. I give up.

plenty of people argue that it might be good sometimes. — unenlightened

You'll have to give me an example of someone arguing that (where 'injustice' refers to the negation of the virtue, not the actual law as it happens to stand). I maintain, for the time being, that no serious moral philosopher, or even people in general, argue that.

The example you gave of extra-judicial killings are people who believe that the law is wrong. That their killings are 'just' in the sense of the virtue, they are merely extra-judicial in the sense of the written law as it happens to stand.

If we allow Anscombe to have some definition of what is 'just', in the sense of the virtue, which is so obvious it doesn't need talking about, then there is no defence at all against charismatic populists adding whatever they like to that definition and immunising themselves from debate on exactly those grounds.

I don't think we have a great deal of defence against charismatic populists as it is, I'm certainly not prepared to go along with throwing away what little we do have.

Isn't the idea of new baboons coming into the tribe and trying to assert dominance then being shunned and shown by the rest "this is not how we do things around here"...a type of pedagogy — ZhouBoTong

No. I'm using pedagogy in it's strict sense here, in that no actual direct teaching took place. Sapolsky even tested directly for this with the tribe when the alpha males first came into it from the nearby Forest Troop. He says

The lack of contingency in thet reatment of transfer males by residents argues against instruction; commensurate with this, there is relatively little evidence for‘‘instruction’’in nonhuman primate cultural transmission — Sapolsky RM, Share LJ (2004) A pacific culture among wild baboons: Its emergence and transmission

Are you a professor? Or some sort of sociology professional? I just mean...why do you know all this? — ZhouBoTong

Yes. I'm sort of retired now, but my academic career has been in social psychology. My wife's a child psychologist though, with a special interest in education, so it's more dinner-table conversation stuff that I've picked this up from, rather than my own work.

should I dismiss Piaget's stages of cognitive development or Erikson's stages of (I don't even remember, maybe social development?)? — ZhouBoTong

Well. That's a whole other thread's worth of stuff - we can go into it any time you like, but probably not on this this thread. Piaget suffers from the same twin problems many of the early child psychologists did - limited sample variety and failure to adjust for context. Margret Donaldson is good on undermining a lot of the Piaget stuff. She doesn't throw it out or anything, but it's remarkable what she gets the children to do (which Piaget said they couldn't) when they're in a less stressful environment. Stephen Shanker is doing some work on the link between stress and educational ability at the moment which might also be of interest, but again, I don't want to derail the thread.

Thank you for the links. I actually had the good fortune to work with one of Kahneman's doctoral students for a short while so I'm fairly familiar with his work, but I will take another look. What I was looking for was some support for your assertions about the possible effects of education, specifically that it "is possible to use education to manifest a culture that promotes morality and decreases social problems." I don't recall anything in Kahneman which demonstrated anything of this nature - could you point me to the particular experiment or implication you're referencing here.

If I could be wrong in believing that Donald Trump is POTUS, then this possibility is contingent upon there being an actual state of affairs — Janus

Not necessarily. It depends if you take a pragmatic definition of 'wrong' or not. Being 'wrong' can amount to nothing more than having a theory which is superseded by a more useful one. I'm not saying that there is no state of affairs, by the way, I think there is. I'm just saying that being 'wrong' need not be contingent on there being one.

Donald Trump being or not being POTUS at the time in question, that would make my belief true or false. — Janus

So, if 'true' is a property of a belief, and a belief is a state of affairs in the brain, a 'true' belief should be distinguishable from a 'false' one one, no? For a belief to have the property of being 'true' (unless we're invoking dualism) it would have to have some physical difference from a false one.

Better, I think, to have 'true' as a category of beliefs, not a property of them. Far less problems with dualism. But if 'true' is a category of belief, then nothing about the real world determines what goes in that category, it's a human-made one. We decide what's in and what's out. Like 'blue'.

This assumes that there is a reality to be perceived or not perceived directly, no? — Janus

Yes. I make that presumption. I don't think we could provide much by way of justification, but I also don't think we're capable of doubting it.