On coronavirus (COVID-19) so far: Part II

The New Neo Posted on by

[NOTE: Part I can be found here.]

While musing about COVID-19, I wondered whether the virus really is novel. Perhaps it’s been around for a while and just wasn’t causing all that many deaths and therefore wasn’t even noticed until the spike occurred in China. Now that the virus has been recognized and is being tested for, perhaps we’re finding it all over the place (in small quantities so far) because it’s long been all over place and not caused all that much damage.

This seemed an odd thought. But it turns out it’s not so odd after all:

…”[H]as this virus ever entered the population undetected and been spreading?” asks Andrew Pekosz, a biologist at the Johns Hopkins Bloomberg School of Public Health. If in previous instances it induced only mild disease, “it may not have registered a large enough number of cases to get on the public health radar screen.”

Ebola and HIV both turned out to have existed for many years before scientists recognized the diseases those viruses cause. Scientists discovered that by running antibody tests on blood that had been stored long ago.

An antibody test is sorely needed, in order to tease out an answer to that question. It would also help us to learn whether there are a great many mild or even symptomless cases that have gone unrecognized, which would change our perception of the lethality of the virus.

There are two main issues with COVID-19, and we don’t know all that much about either yet: contagiousness and lethality. But the situation of the Diamond Princess cruise passengers offers an opportunity to learn about both under a sort of worst case scenario, which is confinement of healthy with ill passengers in a closed system, and an especially susceptible population because of a high percentage of people of advanced age. So let’s take a look.

The first thing you’ll notice is that the headline blares that the ship started with 10 passengers testing positive for the virus and ended with 700 testing positive within the two weeks of the quarantine. That’s quite a leap. The total number of people on the ship was 3,711. So the final number testing positive represented about 19% of the whole, or a little less than a fifth. Of that number – in the month since the first person from the ship was diagnosed – 6 have died, which is .16% of the whole, and .86% of those who tested positive. Both figures are under 1%. That only represents a months’ time, of course, two weeks of which involved quarantine on the ship. But it’s a fairly low figure, especially considering the advanced ages of so many of the passengers. Time will tell whether there will be any more deaths of people who were on that ship.

A large part of the linked article is about the terrible conditions of confinement and fear on the cruise, and how certain things probably fostered the spread of the disease. It’s missing a clear timeline of when people were tested and whether some of the rise in cases over time represented the fact that only certain people were tested at first (perhaps only the symptomatic?). It’s really unclear from the article, and perhaps the health officials on the ship were the ones who were unclear in communicating exactly how the testing went.

This part is especially interesting:

More than half of the infected people (322) showed no symptoms at all, which suggests that some coronavirus carriers in China could be going undetected.

That’s a fact that indicates less mortality – and even less morbidity – than has commonly been reported.

This article also describes the people who died. The first two were 87 and 84, both with underlying pre–existing health issues. The next two were also people in their 80s, and it’s unclear what their previous health status had been. The fifth person was in her 70s, and the sixth was of as-yet unreported age. This is further indication that advanced age is a big factor, just as it is in pneumonia deaths and deaths from most varieties of flu (although not the 1918 flu, where the majority of deaths were of younger adults ).

One question as yet unanswered is, if you eliminate the asymptomatic passengers, what percentage of the others testing positive had only mild symptoms. But we don’t know; at least I haven’t seen this reported, even though it would be important information. This article, based not on the ship data but on Chinese health officials’ reports, says that 80.9% of cases in China have been mild. However, that probably misses almost all the cases that are asymptomatic, and so it doesn’t tell us much about that phenomenon. Of the 19% of confirmed cases in China that have been considered serious, 2.3% were critical, and all the deaths were in that group.

This is how the death rates for COVID-19 so far (mostly in China) compare to previous novel illnesses that have gotten a lot of publicity:

Overall, however, the COVID-19 fatality rate is far lower than that of past coronavirus epidemics. Based on the ratio of deaths to confirmed cases so far, it appears to be about 2%. Severe acute respiratory syndrome (SARS), by contrast, killed 9.6% of those infected, and Middle East respiratory syndrome (MERS) killed 34.4% of cases.

But on the other hand, those illnesses were seemingly less contagious and therefore more easily contained

The following is encouraging, and it makes sense to me:

Fauci and other experts, however, think the existing fatality rate will drop as more mild cases are counted.

And this article points out something that might be obvious but that’s still important to note: novel threats, even if they’re less dangerous than pre-existing threats, can cause more fear. People are used to the familiar.

As I mentioned in Part I, COVID-19 has been hyped by the press and the Democrats, the better to get clicks and/or sell papers, and to criticize and blame Trump. But there’s another factor, which is the increase in our economic dependence on products and shipments from China. That’s real, and any disruption in the supply chain from China could be very problematic. Ironically for the left, another thing Trump’s been doing for quite a while is trying to lessen our trade connection to China. But don’t sit on a hot stove waiting for the left to praise him for it.

Bernie ♥ his myth of Denmark

The New Neo Posted on by

Paul Mirengoff of Powerline points out the ways in which Bernie Sanders’ vision of turning the US into Denmark is a dream based on a myth of what Denmark actually is, and what other Scandinavian countries he admires actually are. In his post, he quotes this op-ed by Fareed Zakaria that appeared in the WaPo:

Take billionaires. Sanders has been clear on the topic: “Billionaires should not exist.” But Sweden and Norway both have more billionaires per capita than the United States — Sweden almost twice as many. Not only that, these billionaires are able to pass on their wealth to their children tax-free. Inheritance taxes in Sweden and Norway are zero, and in Denmark 15 percent. The United States, by contrast, has the fourth-highest estate taxes in the industrialized world at 40 percent.

Zakaria also notes that Sweden, another country much admired by Sanders, had to abandon the sort of economic policies Sanders likes in order to keep itself from going under:

In Sweden, government spending as a percentage of gross domestic product doubled from 1960 to 1980, going from approximately 30 percent to 60 percent. But as Swedish commentator Johan Norberg points out, this experiment in Sanders-style democratic socialism tanked the Swedish economy. Between 1970 and 1995, he notes, Sweden did not create a single net new job in the private sector. In 1991, a free-market prime minister, Carl Bildt, initiated a series of reforms to kick-start the economy. By the mid-2000s, Sweden had cut the size of its government by a third and emerged from its long economic slump.

Mirengoff concludes:

Sanders favors policies much more along the lines of those that failed Scandinavia in the 1960s and 1970s. Or perhaps a mixture of those policies and the ones that are failing in Venezuela today.

You could try running those facts by any Sanders supporters you know. But I wonder whether it would matter to them. I think Sanders’ popularity is a combination of many things, but one of them is that his promises sound well-intentioned and idealistic to his followers, many of whom may not actually expect him to achieve his goals. It’s a sort of virtue-signaling gone wild.

Does Bernie himself even believe that he could accomplish what he promises? I doubt it. But he sounds sincere – at least to his followers. As either Jean Giraudoux or George Burns (quite a combo!) said: “The key to success is sincerity. If you can fake that you’ve got it made.”

Is Sanders faking? I don’t know. But it actually would be better if he were faking, because if he believes his own blather – and somehow manages to convince enough people to get elected – we’d be in even more trouble than if he were just saying it in order to get votes.

What do I think? I think he’s sincerely sincere.

And because in my youth an enormous number of Broadway show tunes became embedded in my head, right after I wrote that last line I thought of this apropos number from “Bye Bye Birdie.” I saw the show in its original run on Broadway at exactly the right age to love it. I had no interest in the movie that came out a few years later, but here it is because the clip features the song I’m talking about. Incidentally – and I only learned this from the YouTube comments – the building in this scene is the same set later used for “Back to the Future”:

New plan: Part II of “On coronavirus (COVID-19) so far” coming tomorrow

The New Neo Posted on by

I thought I’d get Part II of my coronavirus update published today. But in the meantime, I decided to write just a little teeny tiny post on the question of the 1918 flu epidemic and aspirin.

Well, a lot of research and 1525 words later, I’ve decided to hang up my coronavirus-research hat for the day.

That sort of thing happens a lot. I expect a post will be short and easy, like that aspirin one, and it turns out to be anything but.

Aspirin and the 1918 flu death rate

The New Neo Posted on by

Recently there’s been some talk (including in the comments on this blog) of a theory that high doses of aspirin played a key role in exacerbating the number of deaths in the 1918 flu pandemic:

The high case-fatality rate—especially among young adults—during the 1918–1919 influenza pandemic is incompletely understood. Although late deaths showed bacterial pneumonia, early deaths exhibited extremely “wet,” sometimes hemorrhagic lungs. The hypothesis presented herein is that aspirin contributed to the incidence and severity of viral pathology, bacterial infection, and death, because physicians of the day were unaware that the regimens (8.0–31.2 g per day) produce levels associated with hyperventilation and pulmonary edema in 33% and 3% of recipients, respectively. Recently, pulmonary edema was found at autopsy in 46% of 26 salicylate-intoxicated adults. Experimentally, salicylates increase lung fluid and protein levels and impair mucociliary clearance. In 1918, the US Surgeon General, the US Navy, and the Journal of the American Medical Association recommended use of aspirin just before the October death spike. If these recommendations were followed, and if pulmonary edema occurred in 3% of persons, a significant proportion of the deaths may be attributable to aspirin.

I don’t see that it’s especially relevant these days, because no one is recommending doses anywhere near that, and aspirin isn’t as widely used in general even in low doses (except for those who have had cardiovascular problems, who take aspirin in tiny doses to prevent the occurrence of a subsequent event). But putting that aside, I don’t think aspirin was a big deal in the death rate even in 1918, although it might have had some role.

Here’s why I say that:

The international characteristics of the pandemic make the salicylate hypothesis difficult to sustain as the primary explanation for the unusual virulence of the 1918–1919 influenza pandemic. Worldwide, an estimate of the mortality of the 1918–1919 pandemic is 50 million deaths, with a range of up to 100 million deaths. Taking the 50 million figure, this was about 2.5% of the world population. By contrast, in the United States, mortality was on the order of 0.5%. Clearly, the rest of the world was struck more severely, on average, than the United States.

India serves as a useful vignette. Mortality in India was staggering, with estimates of 18.5 million persons dead and higher. Indeed, the Indian peasant population was so severely affected that economics Nobel laureate Theodore W. Schultz used the pandemic as a natural experiment in per capita agricultural output. Given the huge number of deaths in India and the burden among subsistence agricultural workers, it is extremely implausible that salicylates played an exacerbating role in anything other than a trivial percentage of Indian mortality.

Thus, Starko’s intriguing hypothesis fails the test of dose-response. That is to say, in countries such as the United States, where salicylates were more available, mortality was much lower compared with regions where salicylates were less readily available. These observations are at the ecological level, and such comparisons are notoriously susceptible to confounding. However, if the salicylate hypothesis applies universally, then the ecological confounding would have to operate such that the salicylate-influenza connection is stronger in countries with less access to aspirin, which seems a priori unlikely. Indeed, the overwhelming majority of the millions of Indian peasants who were killed by the flu certainly had no access to salicylates whatsoever. If the salicylate hypothesis only works in the United States and in similar settings, then we question its validity given the worldwide scope of severe mortality in 1918–1919.

To summarize: the US had a much lower mortality rate for flu cases in 1918 than a lot of other areas. Of course, as the author of the above quote acknowledges, there may have been (and probably were) many factors that went into that lower mortality. But if in countries where aspirin use was basically nil, the mortality rates were much higher, then it does cut into the likelihood that aspirin was a big factor here, although it doesn’t eliminate it.

One would also have to know how often aspirin actually was used in the US in people who had the 1918 flu. The article speaks of certain spikes in deaths that occurred in waves. But those spikes and waves in which the death tolls were different at different times, even in the same country, are common around the world in flu epidemics. And what’s more, they also occurred in 1918 in other countries where aspirin usage doesn’t seem to have been practiced, much less megadoses of aspirin. It is often part of the natural history of such a disease for its lethality to wax and wane in waves, so attributing that waxing and waning in the US to aspirin usage seems quite iffy to me – especially since we don’t have a good sense of the ways in which aspirin usage waxed and waned in 1918.

And by the way, those mortality figures in the first paragraph of the first quote – 2.5% around the world and .5% in the US – illustrate something I wrote at length about yesterday, which is the confusion that sometimes arises in the reader because mortality percentages can be given in two different ways. To repeat: the figure can represent an illness’ mortality rate as a percentage of the entire population (in a city, a country, or the world). Or, the figure can represent an illness’ mortality rate among those infected (for infectious diseases, of course) or who suffer from it (for a non-infectious disease such as cancer). Quite obviously, the percentages of deaths in the afflicted are significantly higher than in the population as a while. The figures given in the excerpt here are for the percentage of the entire population – that is, 2.5% of the population of the entire world died, and .5% of the population of the US died.

And although the flu was especially bad in India, that country was not even the worst in terms of death rates:

Though other countries lost a higher fraction of their populations—Western Samoa (now Samoa) lost 22 percent, for example, compared to 6 percent in India—because of the larger size of the Indian population, that 6 percent translated into a staggering slew of death. Between 1918 and 1920, an estimated 18 million Indians lost their lives to influenza or its complications, making India the focal point of the disaster in terms of mortality. Asia as a whole experienced some of the highest flu-related death rates in those years, but the story of how the disease ravaged the continent is relatively unknown. The 1918 flu pandemic has been called the “forgotten” pandemic, and ironically the continent that seems to have forgotten it most thoroughly is the one that bore the brunt of it.

And here’s some information about the way that characteristic “wave” pattern I wrote about yesterday operated in 1918, as well as the contagiousness/lethality balance I also mentioned in that earlier post (emphasis mine):

Hunger weakens the immune system, and hunger was rife in many regions of the world in 1918, partly due to disrupted supply lines. Other infectious diseases, such as tuberculosis and typhus, had made inroads into human populations, capitalising on the disruption wrought by war and rendering their victims more vulnerable than usual to a new respiratory infection. Large numbers of people, both troops and refugees, were on the move, providing the ideal vehicle for disseminating that infection. Meanwhile, the very lack of mobility of one group may have helped brew a particularly lethal germ that year, or at least kept it lethal for longer. Once the virus reached the Western Front—the 16-kilometre-wide system of trenches that gashed France from the Belgian to the Swiss border—it encountered large numbers of young men who, packed into those trenches, did not go anywhere for weeks or months. Paul Ewald, an evolutionary biologist at the University of Louisville in Kentucky, has argued that under such exceptional conditions, the evolutionary pressure on the virus to moderate its virulence may have been relieved. It became the mobile one in the host-virus relationship, and it raced through the trenches, killing as it went.

Flu pandemics have a characteristic structure, engulfing the world in waves. The first wave, sometimes called the herald wave, is often quite mild, resembling a seasonal flu. This tends to be followed by a more deadly second wave, and in some cases, subsequent waves of varying severity. The flu pandemic of 1918, though unusually virulent, was no different in this respect. There was a mild herald wave in the northern-hemisphere spring of 1918, a much more lethal second wave in the latter part of that year, and a final recrudescence in the early months of 1919, which was intermediate in severity between the other two. The pattern was repeated in the southern hemisphere, but it was staggered in time with respect to the north, meaning that the waves tended to strike later there. The pandemic is conventionally considered to have been over by March 1920, although earlier this year, the epidemiologist Dennis Shanks and his colleagues at the University of Queensland in Brisbane reported that it dragged on in the Pacific islands for another year, with cases still being reported in New Caledonia in July 1921.

It’s rather complicated, and we’re still learning about it. But if aspirin played much of a role, I think it was a tiny one.

Trump courts more black voters

The New Neo Posted on by

[Hat tip: John Hinderaker at Powerline.]

If this ends up actually working, Democrats will be in trouble:

President Trump is opening 15 urban campaign field offices in an aggressive bid to improve his performance with black voters, who for decades have been an overwhelmingly Democratic constituency.

Sleek and situated in retail shopping districts to generate foot traffic, this unique collection of regional “community centers” is a critical component of the Trump campaign’s multimillion-dollar strategy to double in 2020 the 8% support the president received from black voters nearly four years ago…

Five offices are slated for Florida: Tallahassee, Jacksonville, Orlando, Tampa, and Miami. In North Carolina, branches are opening in Charlotte, Raleigh, and Greensboro. Others will be located in Atlanta, Detroit, Columbus, Cleveland, Philadelphia, Pittsburgh, and Milwaukee.

These cities were probably very carefully chosen, too, as places where changing even a small percentage of black voters’ views to Trump’s side will have the most bang for the buck in terms of being meaningful in winning the state. Note that there are none in New York or California cities. Perhaps the calculation is that that would be wasted effort in states so overwhelmingly blue.

I’ve written before about the effort by Trump – and black conservatives such as Candace Owens – to appeal to black voters. If such a campaign is at all successful, it would be a nightmare for the left. The Democratic Party counts on a nearly monolithic support from black voters to win many states, and any significant defection from that allegiance could be very significant.

Trump is wise to use some resources on this. Perhaps the effort won’t pay off, but if it reaches some sort of critical mass it could be key. Black voters vote Democratic these days in such overwhelming numbers for many reasons, some of it historical and dating back to the 30s and FDR and then the 60s and the Civil Rights legislation. Barack Obama being a Democrat didn’t hurt any, either. But I don’t get the impression that black voters are leftist in ideology, and (as many have pointed out) there is a rather broad streak of social conservation among black voters.

You can see some of the history in this chart:

What you can’t see in that chart is that until FDR, black voters were reliably Republican. You can read a comprehensive article about the switch under FDR here (I haven’t read it). At the time, though, the switch to the Democrats by black voters was just part of a large switch to Democrats among voters generally. It was sparked by the Great Depression and FDR, who received about 61% of the general popular vote in 1936 – and, according to the chart I put up, 71% of the black vote. in 1940 that rose to 62.5% for FDR in the overall vote, and black voters went for him 67%, according to the chart. So, not all that different.

But those percentages for the black voters and the Democratic candidates held, even during the Eisenhower years, and in 1964 there was another huge leap to the almost monolithic Democratic voting among black people that we still see today.

Until now.

It’s an uphill battle. Some of this affiliation with the Democrats is – like most political affiliations – force of habit and surrounding culture. If a person grows up knowing almost all Democrats, it’s hard to break the mold. That’s why black spokespeople such as Owens might be very important.

Here’s a question

The New Neo Posted on by

Are Democratic leaders afraid of Sanders because they don’t want socialism?

Or are they afraid of him because they think he’s too open about his plans for socialism, and they think that would ruin his chances for election and would lead to Trump’s second term and perhaps even the flipping of the House?

I’ll tell you my answer: for the majority, it’s the second. But for a dwindling few, it’s the first.

On coronavirus (COVID-19) so far [Part I]

The New Neo Posted on by

[NOTE: I’ve decided this needs to be at least a two-parter, because there’s so much to be said. Here’s Part I.]

I haven’t written too many posts on the new coronavirus (COVID-19) because we know quite little, and much of what we read about it in the MSM probably is incorrect. Nevertheless, it’s what we have to work with right now.

You keep hearing “don’t trust the Chinese on this.” And I agree. But that also means that we can’t trust the people who at least theoretically know the most about it, because they’ve had the largest numbers of cases. And it also sets the scene for cinematic apocalyptic imaginings to rush in, ideas that many in the MSM are only too happy to entertain, the better to raise ratings and to hurt Trump. A twofer.

Prognosticators don’t want to be caught flat-footed if this becomes a much much bigger deal than it already is. People have learned more and more in recent years not to trust governments and bureaus and bureaucrats. So all of that is operating, too.

But here’s what I’ve gleaned so far.

First, some general statements. I’ve read that for infectious diseases, lethality and ease of contagion are ordinarily (not always) somewhat in opposition. That makes sense, because if a disease is quickly and highly lethal, the sufferer will have much less opportunity to be walking around with it in his or her most contagious stages, and therefore will tend to infect fewer people.

That’s why many illnesses that are highly widespread – take the common cold, which is called “common” for a reason – are usually mild (although tell that to the cold sufferer). And yet even such seemingly innocuous illnesses have some lethality, in that (for example) a cold can lead in the susceptible to pneumonia, which is far more likely to kill.

Pneumonia is something we’re all familiar with because, like the common cold, it’s reached a relatively stable rate of infection and, although far less common than the cold, it’s something not especially uncommon. And unlike COVID-19, it’s far from new. But pneumonia can kill, and you might be surprised to learn how often. Pneumonia statistics are as follows:

For US adults, pneumonia is the most common cause of hospital admissions other than women giving birth. About 1 million adults in the US seek care in a hospital due to pneumonia every year, and 50,000 die from this disease.

That’s a death rate of 5%. And not all these people are old or ill to begin with, either (see the link for more), although many are.

I’ve also seen discussions of the 1918 flu in comparison with COVID-19. The 1918 flu was a pandemic, both worldwide and more lethal than ordinary flu (which can also kill). And the death rate in 1918? The truth is that no one really knows what the death rate was in those who contracted the disease. One reason is that in those days, reporting rules were often nonexistent, even in the US. Here’s an account that focuses on the state of Washington, for example (the term “Spanish flu” is used in the excerpt, and although this is a misnomer it was a common term for it):

For several reasons, tracking the progress of the pandemic in the state with much accuracy is impossible. First, influenza was not a disease that had to be reported to state health authorities, at least not during its most virulent phase in the fall of 1918. Voluntary reporting was extremely sporadic, as will be seen. Deaths needed no diagnosis and were faithfully recorded, but overall tallies of the infected must be considered rough estimates, even when impressively specific.

Second, the flu in 1918 and early 1919 came in three distinct waves — a usually mild form in the spring and summer of 1918, followed by the deadly strain in the closing months of that year, and ending with a return of usually (but not always) milder disease in the early months of 1919, not fully tapering off until 1920.

To further frustrate public-health authorities, the Spanish flu killed both directly and by leaving victims vulnerable to secondary infections with bacterial pneumonia, which was often fatal even in the absence of the flu, particularly in the elderly or infirm. This muddled the causality picture. But because the Spanish flu had proven so stunningly contagious and pneumonia was so often found during autopsies of flu victims, the federal Census Bureau decided to use a single category in its mortality statistics for 1918: “deaths from influenza and pneumonia (all forms)” (Mortality Statistics, 1918). As frustrating as it is to epidemiologists and life-insurance actuaries, all statistical studies of the effects of the 1918 pandemic are riddled with uncertainty and approximations.

The difficulties are obvious. And that passage describes the situation in the US, which had relatively good reporting (and probably lower death rates as well) compared to so many other countries:

Although the death toll attributed to the Spanish flu is often estimated at 20 million to 50 million victims worldwide, other estimates run as high as 100 million victims—around 3 percent of the world’s population. The exact numbers are impossible to know due to a lack of medical record-keeping in many places.

What’s more – and what can be confusing – death rates can refer to two different things. The first one is the overall death rate from the disease in the general population, and the second is the death rate from the disease in all people infected with it.

More about the death rate in 1918, which not only is unknowable for sure but seems to have varied widely by country:

Worldwide, an estimate of the mortality of the 1918–1919 pandemic is 50 million deaths, with a range of up to 100 million deaths. Taking the 50 million figure, this was about 2.5% of the world population. By contrast, in the United States, mortality was on the order of 0.5%. Clearly, the rest of the world was struck more severely, on average, than the United States.

So, if 2.5% of the world’s entire population died (and that’s using the lower total death figure of 50 million), we can safely say that the death rate in those infected had to have been way higher. This estimate is that about a quarter of the world’s population contracted the 1918 illness, and the death rate in the entire population from it was 2.8%, which by my calculations would give a death rate in the infected of four times that, which would be somewhere (using 2.5% or 2.8%) between 10 or around 11 per cent. That’s very high, much higher than anything that’s been reported for COVID-19 so far. It seems that the 1918 flu had some highly unusual characteristic for flu, which was that it was both very contagious and unusually lethal. It also happened to have killed a disproportionate number of people in the prime of life rather than just the very old or very young, which does not seem to match the COVID-19 pattern so far either.

Most estimates I’ve seen so far about the death rate in COVID-19 are that it’s around 2.5% of people who are infected (not of the general population). However, there are several possible problems with this. One is that doctors may be missing a large number of mild or even asymptomatic cases, which would make the actual death rate much lower than that. Another is that it’s not just the death rate but the pattern of deaths that’s important. Most of the deaths have occured in the elderly and especially the very elderly. And almost all of them (so far) have been in China. Obviously, the death toll will keep rising, and not just in China, but we don’t know at what rate. We also don’t know whether the geographic pattern will continue, or whether reports that infection rates may be going down in China are true or not.

Italy has more cases than other countries in Europe right now. This is especially mysterious. But it may have something to do with this [emphasis mine]:

More than 3,000 tests for coronavirus have been carried out [in Italy] over the last few days, although authorities are still trying to identity “patient zero” – the person who brought the virus to the region. The first man infected, a researcher at Unilever, came down with symptoms after attending a dinner at which there was a colleague who had recently returned from China, who tested negative for the virus.

“The peak in Italy is partly due to all the tests being done,” said Roberta Siliquini, a former president of Italy’s higher health council. “We have found positive cases in people who probably had few or no symptoms and who may have overcome the virus without even knowing it.”

The Italian government has been criticised for hastily cancelling flights to and from China as, without coherence across Europe, people have been able to fly to other European cities and enter Italy from there.

That’s because Europe has open borders, so if some European countries are letting people in from China, this affects every country in Europe and it’s hard if not impossible to trace whether people have had any contact with anyone who recently came back from China.

I’ll add just one more thing, and then close Part I down, because it’s already way long. Despite rumors and even reports of transmission when people are asymptomatic, there’s no hard evidence of it so far. That doesn’t mean it’s not happening.

Reading Maus

The New Neo Posted on by

[NOTE: Years ago I downsized and got rid of a lot of books. But since I’d had a ton of them to begin with, I’ve still got a lot, although nothing like the original number. And of course, I keep adding to them, although not at a very fast clip; I try to use the library most of the time. I don’t like Kindles or audiobooks, so when I purchase a book it’s always a real three-dimensional book of the old-fashioned kind.

The other night I was up late looking for a certain book and couldn’t find it. As I searched, I discovered that I was missing about six key books in my library. So I set about asking some close friends if they might have them, since I sometimes lend such things and lose track. Sure enough, a few of the books came back to me. One was the first volume of the graphic novel Maus.

That motivated me to look up an old post I’d written, a review of the book. And reading it made me decide to publish it again. So here it is.]

I recently reread the two-volume graphic novel Maus, by Art Spiegelman. It struck me once again, as it did the first time I read these books, that they should not work on any level. And yet, against all odds, they constitute a bona fide masterpiece.

Why should they fail? Let me count the ways. Because of our over-familiarity with the genre, as well as the risk of trivialization, Holocaust stories are inherently difficult to write, especially by people such as Spiegelman who did not directly experience the horrors. He chooses to write in the form of the graphic novel—in other words, a lengthy cartoon. This genre should be especially offensive as a medium for telling so deeply horrific and monumental a tale.

What’s more, Spiegelman decides to depict the protagonists as various animals, which might have served to underline the cartoon aspects as well as dehumanizing the story: the hunted Jews are mice, the Nazis are cats, Poles are pigs, Russians bears, Americans dogs. And he intersperses his own experience of typical and somewhat pedestrian intergenerational angst and parent-child strife with the searing Holocaust sufferings of his parents.

How is it that Spiegelman manages to succeed? He begins slowly, by introducing his father Vladek but concentrating on their present-day post-Holocaust American life (the book was first published in the mid-80s). The man is so crotchety and annoying, so stingy and testy, that the reader shares Spiegelman’s frustration with him. And then the son gets the idea of interviewing his father about his experiences during the war, and the story begins to shift gear into a very different time and place.

Part of the power of the book comes from the idiosyncratic, colorful, and yet laconic way Vladek expresses himself, in accented English that conveys his practical and canny nature. The use of animals to portray the different ethnic and national groups stops seeming strange and becomes powerfully symbolic, keeping the reader from ever forgetting for a moment that these identities were the most salient characteristics of the world in which Vladek and his fellows lived, marking him and his fellow Jews as hunted prey and others as predators, helpers, or neutrals.

The reader learns at the outset that Spiegelman’s mother is dead. Although she came through the Holocaust seemingly intact, she committed suicide when Art was a young adult. As Vladek’s story introduces the reader slowly to the person she was, it becomes more and more apparent that the love between the two was an extraordinarily powerful force, and largely responsible for her wartime survival. Vladek was able to at least temporarily transfer some of his own remarkable gift for endurance to his wife. He was very clever and resourceful. But “clever” and “resourceful” are mild words to describe his stunning ability to find a way out of almost any situation.

Virtually all Holocaust survivor stories involve large elements of both luck and skill. But, having read many such tales, I think I can safely say that Vladek’s history involves more of the latter than any other such story I have read. He is always planning ahead, always thinking, always ingratiating himself with those who might be able to help him in the future. He pretends to have knowledge and training he lacks, and then he makes it his business to learn those skills and to learn them quickly and well (shoemaking, tinsmithing). Although starving, he manages the extraordinary feat of controlling his hunger in order to save food to use as bribes or gifts in ways that can help him in the future.

As Vladek’s past emerges in his own words, the reader—and his son Art—learn the source of many of the man’s maddening quirks. What appears from the perspective of the bountiful America of the 1980s to be a miserly and rather nasty need on the old man’s part to save and hoard seemingly useless things is revealed to be the same impulse that allowed him to live while so many others died. The angry Vladek who is so mean to his second wife (another Holocaust survivor) still mourns the first wife he loved so deeply. The man who maddens son Art with his clinginess and demands is the same person who lost almost every member of his large family, including his first child, in ways that retain their power to horrify even those who are familiar with the Holocaust.

It is said that to know all is to understand all. By the time Art has finished interviewing his father and writing the book, he has come to understand as best he (or any other person who did not directly experience the Holocaust) can what motivates the man, and to respect those very traits of his that originally drove the son nearly crazy. In one of the final panels of the book, Vladek, now very ill and lying in bed, sleepily addresses Art by the name of his deceased first son Richieu who died as a young child in the war. This especially moving moment demonstrates the fusion of the past with the present, and the fact that the dead still exist in the mind, untethered to time.

The strength of Maus is that it tells two tales simultaneously: an almost unimaginably terrifying story of suffering and heroic survival is interspersed with the story of the ordinary middle class life of an American family in which Old World parents give birth to a New World son. No one is spared and no one is glorified, and yet the final message amidst the horror and cynicism is of the power and depth of love.

On coronavirus COVID-19

The New Neo Posted on by

I wrote a rough draft last night for a huge post about coronavirus. But I got a very late start today due to an excess of busyness with other, non-blog things, as well as other topics and posts.

It happens sometimes.

So that coronavirus post isn’t coming today. But I just wanted to let you know that I’m not ignoring the topic, and that a post or maybe even a 2-parter should be coming soon.

You can talk about COVID-19 here, though, if you like. A very very short summary of my stance at the moment is that (a) we don’t know much (b) and yet there’s a ton of misinformation and/or misleading information out there; and (c) a lot of people are trying to stir up premature panic, and have been quite successful in doing so.

Lots of facts about marijuana

The New Neo Posted on by

I happen to have come across this article about the state of knowledge on marijuana, now that it’s legal in so many states. It is an interview with Kevin Hill, associate professor of psychiatry at Harvard Medical School and director of the Division of Addiction Psychiatry at Beth Israel Deaconess Medical Center. The following are some excerpts from Hill’s remarks:

We know a lot more about both the benefits and the risks of cannabis use, although I would say that the rate and scale of research has not kept pace with the interest…

Unfortunately, the loudest voices in the cannabis debate often are people who have political or financial skin in the game, and the two sides are entrenched. Pro-cannabis people will say that cannabis is the greatest medication ever, and harmless. Others — often in the same field that I’m in, people who treat patients, people who do research with cannabis — will at times misrepresent the facts as well…

I think the greatest example is when you talk about the addictive nature of cannabis. You can become addicted to cannabis, though most people don’t…It’s less addictive than alcohol, less addictive than opioids, but just because it’s less addictive doesn’t mean that it’s not addictive. There’s a subset of people — whom I treat frequently — who are using cannabis to the detriment of work, school, and relationships…I often compare cannabis to alcohol. They’re very similar in that most people who use never need to see somebody like me. But the difference is that we all recognize the dangers of alcohol. If you go into a room of 200 high school kids, they know it’s dangerous and binge drinking among high schoolers is way down. But if you ask that same group about cannabis, you’re going to get all different answers. Data that suggests that although cannabis use among young people is flat — that’s another misrepresentation, that it’s going up — the perception of risk among those young people is going down. So, while everyone’s talking about it, and stores are opening in Brookline, in Leicester, and all over the state, adults and young people are not clear about the risks.

There’s a great deal more at the link. I suggest, if you’re interested in the topic – which I certainly am – that you read the whole thing.