Rob Bensinger

Communications lead at MIRI. Unless otherwise indicated, my posts and comments here reflect my own views, and not necessarily my employer's.

Rob Bensinger's Comments

Rob Bensinger's COVID-19 overview

[Copy of the Apr. 26 section "Maybe stop taking ibuprofen/advil?", deleted from the main text Jun. 2. A still earlier version just said that some sources were warning about NSAIDs and to therefore avoid them out of an abundance of caution.]

Fang et al. write in The Lancet:

Human pathogenic coronaviruses (severe acute respiratory syndrome coronavirus [SARS-CoV] and SARSCoV-2) bind to their target cells through angiotensin-converting enzyme 2 (ACE2), which is expressed by epithelial cells of the lung, intestine, kidney, and blood vessels.[4] The expression of ACE2 is substantially increased in patients with type 1 or type 2 diabetes, who are treated with ACE inhibitors and angiotensin II type-I receptor blockers (ARBs).[4] Hypertension is also treated with ACE inhibitors and ARBs, which results in an upregulation of ACE2.[5] ACE2 can also be increased by thiazolidinediones and ibuprofen. These data suggest that ACE2 expression is increased in diabetes and treatment with ACE inhibitors and ARBs increases ACE2 expression. Consequently, the increased expression of ACE2 would facilitate infection with COVID-19. We therefore hypothesise that diabetes and hypertension treatment with ACE2-stimulating drugs increases the risk of developing severe and fatal COVID-19.

Qiao et al. conclude that ibuprofen enhances ACE2 in diabetic rats. Qiao et al. is the only study I've seen on 'ibuprofen increases ACE2', and this claim is uncited in Fang et al. The ibuprofen-ACE2-COVID link doesn't seem to be widely known / accepted / cared about, based on the discussion on Science Translational Medicine (which argues increased ACE2 might reduce COVID-19 severity; see also the comment section) and Snopes. I also don't know whether I should expect other NSAIDs to interact with ACE2 in the same way as ibuprofen.

On Mar. 14, Samira Jeimy wrote: "In Germany and France, ICU physicians have noticed that the common thread amongst young patients needing #COVIDー19 related ICU admission is that they had been using NSAIDS (Advil, Motrin, Aleve, Aspirin)." She cites the Lancet paper and Day:

Scientists and senior doctors have backed claims by France’s health minister that people showing symptoms of covid-19 should use paracetamol (acetaminophen) rather than ibuprofen, a drug they said might exacerbate the condition.

The minister, Oliver Veran, tweeted on Saturday 14 March that people with suspected covid-19 should avoid anti-inflammatory drugs. “Taking anti-inflammatory drugs (ibuprofen, cortisone . . .) could be an aggravating factor for the infection. If you have a fever, take paracetamol,” he said.

His comments seem to have stemmed in part from remarks attributed to an infectious diseases doctor in south west France. She was reported to have cited four cases of young patients with covid-19 and no underlying health problems who went on to develop serious symptoms after using non-steroidal anti-inflammatory drugs (NSAIDs) in the early stage of their symptoms. The hospital posted a comment saying that public discussion of individual cases was inappropriate.

But Jean-Louis Montastruc, a professor of medical and clinical pharmacology at the Central University Hospital in Toulouse, said that such deleterious effects from NSAIDS would not be a surprise given that since 2019, on the advice of the National Agency for the Safety of Medicines and Health Products, French health workers have been told not to treat fever or infections with ibuprofen.

Experts in the UK backed this sentiment. Paul Little, a professor of primary care research at the University of Southampton, said that there was good evidence “that prolonged illness or the complications of respiratory infections may be more common when NSAIDs are used—both respiratory or septic complications and cardiovascular complications.”

He added, “The finding in two randomised trials that advice to use ibuprofen results in more severe illness or complications helps confirm that the association seen in observational studies is indeed likely to be causal. Advice to use paracetamol is also less likely to result in complications.”

Ian Jones, a professor of virology at the University of Reading, said that ibuprofen’s anti-inflammatory properties could “dampen down” the immune system, which could slow the recovery process. He added that it was likely, based on similarities between the new virus (SARS-CoV-2) and SARS I, that covid-19 reduces a key enzyme that part regulates the water and salt concentration in the blood and could contribute to the pneumonia seen in extreme cases. “Ibuprofen aggravates this, while paracetamol does not,” he said.

Charlotte Warren-Gash, associate professor of epidemiology at the London School of Hygiene and Tropical Medicine, said: “For covid-19, research is needed into the effects of specific NSAIDs among people with different underlying health conditions. In the meantime, for treating symptoms such as fever and sore throat, it seems sensible to stick to paracetamol as first choice.” [...]

The Snopes page above cites Tom Wingfield saying:

In the UK, paracetamol would generally be preferred over non-steroidal anti-inflammatory drugs (“NSAIDS”) such as ibuprofen to relieve symptoms caused by infection such as fever. This is because, when taken according to the manufacturer’s and/or a health professional’s instructions in terms of timing and maximum dosage, it is less likely to cause side effects. Side effects associated with NSAIDs such as ibuprofen, especially if taken regularly for a prolonged period, are stomach irritation and stress on the kidneys, which can be more severe in people who already have stomach or kidney issues. It is not clear from the French Minister’s comments whether the advice given is generic ‘good practice’ guidance or specifically related to data emerging from cases of Covid-19 but this might become clear in due course.

So most sources seem to agree that acetaminophen is at least a bit better than ibuprofen for treating fever-causing illnesses in general; but there's confusion and disagreement about whether ibuprofen is unusually good or bad for COVID-19 in particular, and I don't get the sense using ibuprofen is widely seen as a terrible idea. Elizabeth van Nostrand writes, "France is recommending against NSAIDs and against ibuprofen in particular. I will be very surprised if that ends up being born out (and WHO agrees with me)". 

Overall, the evidence is such that I'm avoiding ibuprofen right now, but I wouldn't recommend going to huge lengths to avoid ibuprofen.

See 3E below on whether and when it's a good idea to manually reduce fevers at all.

Rob Bensinger's COVID-19 overview

Updates, June 2:


2A. Avoid people, especially indoors.

[Section renamed from "Avoid people."]

[Deleted the CDC quote that COVID-19 is mainly spread "between people who are in close contact with one another (within about 6 feet)", per Zvi's criticism of the meme.]


2B. If you do need to be around people, face away from them, minimize talking, etc.

[New section.]

Jonathan Kay writes on Apr. 23,

According to the binary model established in the 1930s, droplets typically are classified as either (1) large globules of the Flüggian variety—arcing through the air like a tennis ball until gravity brings them down to Earth; or (2) smaller particles, less than five to 10 micrometers in diameter (roughly a 10th the width of a human hair), which drift lazily through the air as fine aerosols.

[...] Despite the passage of four months since the first known human cases of COVID-19, our public-health officials remain committed to policies that reflect no clear understanding as to whether it is one-off ballistic droplet payloads or clouds of fine aerosols that pose the greatest risk—or even how these two modes compare to the possibility of indirect infection through contaminated surfaces (known as “fomites”).

Gaining such an understanding is absolutely critical to the task of tailoring emerging public-health measures and workplace policies, because the process of policy optimization depends entirely on which mechanism (if any) is dominant:

1. If large droplets are found to be a dominant mode of transmission, then the expanded use of masks and social distancing is critical, because the threat will be understood as emerging from the ballistic droplet flight connected to sneezing, coughing, and laboured breathing. We would also be urged to speak softly, avoid “coughing, blowing and sneezing,” or exhibiting any kind of agitated respiratory state in public, and angle their mouths downward when speaking.

2. If lingering clouds of tiny aerosol droplets are found to be a dominant mode of transmission, on the other hand, then the focus on sneeze ballistics and the precise geometric delineation of social distancing protocols become somewhat less important—since particles that remain indefinitely suspended in an airborne state can travel over large distances through the normal processes of natural convection and gas diffusion. In this case, we would need to prioritize the use of outdoor spaces (where aerosols are more quickly swept away) and improve the ventilation of indoor spaces.

3. If contaminated surfaces are found to be a dominant mode of transmission, then we would need to continue, and even expand, our current practice of fastidiously washing hands following contact with store-bought items and other outside surfaces; as well as wiping down delivered items with bleach solution or other disinfectants.

Zvi Mowshowitz comments:

Identified Super Spreader Events are Primarily Large Droplet Transmission

The article makes a strong case that in identified super spreader events [SSEs] the primary mode of transmission is large droplets. And that large droplets are spread in close proximity, by people talking (basically everything) or singing (several choir/singing practices) frequently or loudly, or laughing (many parties) and crying (funerals), or otherwise exhaling rapidly (e.g. the curling match) and so on.

There is a highly noticeable absence of SSEs that would suggest other transmission mechanisms. Subways and other public transit aren’t present, airplanes mostly aren’t present. Performances and showings of all kinds also aren’t present. Quiet work spaces aren’t present, loud ones (where you have to yell in people’s faces) do show up. University SSEs are not linked to classes (where essentially only the professor talks, mostly) but rather to socializing. [...]

Zvi argues that surfaces and small aerosolized droplets are unlikely to be major infection vectors for COVID-19. He discusses methods for avoiding large droplet transmission:

Large Droplets: Six Foot Rule is Understandable, But Also Obvious Nonsense

For large droplets, there is essentially zero messaging about angling downwards or avoiding physical actions that would expel more droplets, or avoiding being in the direct path of other people’s potential droplets.

Instead, we have been told to keep a distance of six feet from other people. We’ve told them that six feet apart is safe, and five feet apart is unsafe. Because the virus can only travel six feet.

That’s obvious nonsense. It is very clear that droplets can go much farther than six feet. Even more than that, the concept of a boolean risk function [i.e., one that sharply divides everything into either "risky" or "risk-free", with no shades of grey] is insane. People expel virus at different velocities, from different heights, under different wind conditions and so on. The physics of each situation will differ. The closer you are, the more risk.

Intuitively it makes sense to think about something like an inverse square law until proven otherwise, so six feet away is about 3% of the risk of one foot away. That’s definitely not right, but it’s the guess I feel comfortable operating with.

Alas, that’s not the message. The message is 72 inches safe, 71 inches unsafe.

Unlike the previous case of obvious nonsense, there is a reasonable justification for this one. I am sympathetic. You get about five words. “Always stay six feet apart” is a pretty good five words. There might not be a better one. Six feet is a distance that you can plausibly mandate and still allow conversations and lines that are moderately sane, so it’s a reasonable compromise.

It’s a lie. It’s not real. As a pragmatic choice, it’s not bad.

The problem is it is being treated as literally real.

Joe Biden and Bernie Sanders met on a debate stage. The diagram plans had them exactly six feet apart.

In an article, someone invites the author, a reporter, to their house to chat. Says he’s prepared two chairs, six feet apart. “I measured them myself,” he says. [...]

And so on. People really are trying to make the distance exactly six feet as often as possible.

[...] This is society sacrificing bandwidth to get a message across. Again, I get it. The problem is we are also sacrificing any ability to convey nuance. We are incapable, after making this sacrifice, of telling people there is a physical world they might want to think about how to optimize. There is only a rule from on high, The Rule of Six Feet.

Thus, we may never be able to get people to talk softly into the ground rather than directly looking at each other and loudly and forcefully to ‘make up for’ the exact six foot distance, which happens to be the worst possible orientation that isn’t closer than six feet. 

In theory, we can go beyond this. You get infected because droplets from an infected person travel out of their face and touch your face.

Thus, a line is remarkably safe if everyone faces the same way, modulo any strong winds. The person behind you has no vector to get to your face. And we can extend that. We can have one sidewalk where people walk north, and another on the other side of the street where people walk south. If you see someone approaching from the other direction, turn around and walk backwards while they ensure the two of you don’t collide. If necessary, stand in place for that reason. Either way, it should help – if this is the mechanism we are worried about. 

[...] Yes, it’s annoying to not face other people, but you absolutely can have a conversation while facing away from each other. It’s a small price to pay.

In similar fashion, it seems a small price to pay to shut the hell up whenever possible, while out in public. Talking at all, when around those outside your household, can be considered harmful and kept to a bare minimum outright (and also it should be done while facing no one).

Zvi emphasizes that there’s much more benefit to slightly reducing the risk from the largest infection sources (including large droplets as a category), than from hugely reducing the risk from fairly unlikely infection sources:

Focus Only On What Matters

[...] Within those big risks, small changes matter. They matter more than avoiding small risks entirely.

A single social event, like a funeral, birthday party or wedding, might well by default give any given person a 30%+ rate to infect any given other person at that event if the event is small, and a reasonably big one even if large. You only need one. Keeping slightly more distance, speaking slightly less loudly, and so on, at one such event, is a big risk reduction. [...]

Whereas a ‘close contact’ that doesn’t involve talking or close interaction probably gives more like (spitballing a guess, but based on various things) an 0.03% rate of infection if the other person is positive, and likely with a lower resulting viral load. Certainly those contacts add up, but not that fast. Thus, a subway car full of “close contact” might give you 10 of them per day, most of whom are not, at any given time, infectious. If this model is correct. 

In another post, Zvi writes:

Risks Follow Power Laws

[...] Slight reductions in the frequency and severity of your very risky actions is much more important than reducing the frequency of nominally risky actions.

The few times you end up talking directly with someone in the course of business, the one social gathering you attend, the one overly crowded store you had to walk through, will dominate your risk profile. Be paranoid about that, and think how to make it less risky, or ideally avoid it. Don’t sweat the small stuff.

And think about the physical world and what’s actually happening around you!


My best guess is there is something like 5-10 times as much risk indoors versus the same activity outdoors. [...]

The combination of quick and outdoors and not-in-your-face probably effectively adds up to safe, especially if you add in masks. During the peak epidemic in New York things were so intense that it would have been reasonable to worry about miasma. Now, I would do my best to keep my distance and avoid talking at each other, but mostly not worry about incidental interactions.

I do expect there to be a spike in cases as the result of protests and civil unrest.. To not see one would be surprising, and would update me in favor of outdoor activities being almost entirely harmless.


2C. If you do need to be around people, wear something over your mouth and nose.

[Deleted the advice for individuals not to buy medical-grade masks because it doesn't currently seem like good advice (and I'm not particularly convinced it was ever good advice).]

Zvi Mowshowitz writes, “[E]ven cloth masks on both ends of an interaction are almost certainly good for a 25% reduction in risk and probably 50%-75%.”


2D. Don’t put coronavirus in your face.

Zvi Mowshowitz argues:

It’s been months. We don’t have concrete examples of infection via surfaces. At all. It increasingly seems like while such a route is possible, and must occasionally happen, getting enough virus to cause an infection, in a live state, via this route, is very hard. When you wash your hands and don’t touch your face, it’s even harder than that.

Meanwhile, those who refuse to touch surfaces like a pizza delivery box end up in more crowded locations like grocery stores, resulting in orders of magnitude more overall risk.

[...] Until I get very unexpected evidence, surfaces are mostly not a thing anymore. If lots of people touch stuff and then you touch it, sure, wash your hands after and be extra careful to not touch your face in the interim. Otherwise, stop worrying about it.

[... Food] is at most minimally risky, even if it doesn’t get heated enough to reliably and fully kill the virus. You don’t have to ruin all your food. People are often avoiding foods that seem risky. Once again, it makes sense that it could be risky, but in practice it’s been months and it does not seem to work that way. The precautions people are taking will incidentally be more than good enough to guard against contamination of food at sufficient levels to be worth worrying about. I mean, sure, don’t eat at a buffet, but it’s not like any of them are going to be open, and even then the (also mostly safe) surfaces are likely scarier than the food.

[...] Your risk is from the waiter, or from the other diners, being in that room with you for a while. Thus, takeout, delivery and/or eating outdoors.

I agree with Zvi that it seems increasingly likely that surface transmission is rare, though he seems to be wrong that there are no examples (see comments), and I haven’t seen a clear argument for whether the number of COVID-19 cases caused by surface transmission is closer to 1/10 of all cases versus, say, 1/10,000. Given my own circumstances, I’m likely to do things like “order delivery pizza” more often in the weeks to come, but I’ll also likely make use of Yao Lu’s tips while infections are still commonplace in my part of the US:

I’m a chemo nurse, this is what I tell my high-risk patients:

I personally don’t trust takeout that much because I think a lot of restaurant workers don’t have sick leave, so it’s more likely your food was prepared by someone symptomatic. But you can cut the risk to near zero by doing this:

1. Wash your hands well

2. Put your own bowl on your kitchen counter

3. Pick up the restaurant container, and pour the food into your own bowl

4. Throw away the restaurant container

5. Wash your hands well

6. Thoroughly heat up the food. (at least 70C for a minute, or whatever the best current guideline says)

If you do this, in this order, you are extremely safe even if someone coughed viruses all over the food and the container. Heat would kill the virus, and handwashing would prevent indirect transmission from the bag/container.


2G. Disinfect surfaces.

See also Zvi Mowshowitz’s recommendations to worry less about surfaces, quoted above.


2H. Maybe stop taking ibuprofen/advil?

[Deleted this section because the post is getting long and this seems messy and uncertain. I'll reproduce the Apr. 26 version of the section in a reply to this comment for when I want to link directly to it.]


2J. Run an air filter.

[Provisionally deleted "Also, quit smoking." because I haven't been keeping up with the debate about cigarettes or nicotine.]


3A. Prepare in advance.

Plan in advance what hospital you’ll go to if necessary, and be ready to call a doctor if you have troubling symptoms. Zvi Mowshowitz writes:

Medical care matters [for fatality rates]. Total breakdown of medical care in practice leads to several times the fatality rate under regular circumstances. High quality treatment at current knowledge levels can probably drive death rates down further, so the ratio between full success and complete breakdown can be rather large – something like an order-of-magnitude difference between 0.2% and 2%.

I don’t have a strong opinion at this point about particular medical treatments beyond the above.


3G. Monitor for clotting problems.

Jim Babcock said on Apr. 28,

My first-pass literature review turned up some claimed mechanisms by which platelets and clotting may serve an immune purpose. I don't know if that's what happening here, but there's a possibility that this works like fever reduction: helpful in extreme cases, bad in minor cases and early in the progression.

Low-dose heparin seems to be common hospital protocol now, so data should be forthcoming for that scenario. I don't know what recommendation to give to minor cases self-treating at home, though.

[I meant to add the above before, but forgot about it. This is part of why I withdrew the recommendation that people take aspirin at home whenever they start showing COVID-19 symptoms.]

Possible takeaways from the coronavirus pandemic for slow AI takeoff

Yeah, I've seen that photo before; I'm glad we have a record of this kind of thing! It doesn't cause me to think that the thing I said in 2017 was false, though it suggests to me that most FHI staff overall in 2014 (like most 80K staff in 2017) probably would have assigned <10% probability to AGI-caused extinction (assuming there weren't a bunch of FHI staff thinking "AGI is a lot more likely to cause non-extinction existential catastrophes" and/or "AGI has a decent chance of destroying the world, but we definitely won't reach AGI this century").

Possible takeaways from the coronavirus pandemic for slow AI takeoff

In September 2017, based on some conversations with MIRI and non-MIRI folks, I wrote:

I think that at least 80% of the AI safety researchers at MIRI, FHI, CHAI, OpenAI, and DeepMind would currently assign a >10% probability to this claim: "The research community will fail to solve one or more technical AI safety problems, and as a consequence there will be a permanent and drastic reduction in the amount of value in our future."

People may have become more optimistic since then, but most people falling in the 1-10% range would still surprise me a lot. (Even excluding MIRI people, whose current probabilities I don't know but who I think of as skewing pessimistic compared to other orgs.)

80,000 Hours, based on interviews with multiple AI risk researchers, said "We estimate that the risk of a serious catastrophe caused by machine intelligence within the next 100 years is between 1 and 10%."

I complained to 80K about this back in 2017 too! :) I think 1-10% here was primarily meant to represent the median view of the 80,000 Hours team (or something to that effect), not the median view of AGI safety researchers. (Though obviously 80,000 Hours spent tons of time talking to safety researchers and taking those views into account. I just want to distinguish "this is our median view after talking to experts" from "this is our attempt to summarize experts' median view after talking to experts".)

Covid-19: My Current Model
Predictions Updates
1. Bay Area lockdown (eg restaurants closed) will be extended beyond June 15: 60%
I sold to 40%.

Since this section is called "Prediction Updates", I initially thought you were saying you'd predicted 60% on May 1, and are now predicting 40%. You may want to clarify that 60% was Scott's April 29 prediction, and 40% was your May 1 prediction.

Covid-19: My Current Model
It’s been months. We don’t have concrete examples of infection via surfaces. At all. It increasingly seems like while such a route is possible, and must occasionally happen, getting enough virus to cause an infection, in a live state, via this route, is very hard.

On April 23 I wrote on Facebook:

For most things, I'm just leaving it to air out for 3+ days. If I need to put it in the fridge or freezer, I disinfect it first.

My gestalt amateur sense is that surface transmission from people you aren't spending a bunch of in-person time with seems really low. (Do we even know of any clear examples of this, for COVID-19?) But I'm in a dusty/moldy house in a remote area with no nearby ICUs, so I'd rather err on the side of caution.

(The dust thing seems less important to me now that I'm thinking of COVID-19 as disproportionately endangering people who have cardiovascular issues, not so much people who have respiratory issues.)

Eloise Rosen replied:

> Do we even know of any clear examples of this, for COVID-19?
"A woman aged 55 years (patient A1) and a man aged 56 years (patient A2) were tourists from Wuhan, China, who arrived in Singapore on January 19. They visited a local church the same day and had symptom onset on January 22 (patient A1) and January 24 (patient A2). Three other persons, a man aged 53 years (patient A3), a woman aged 39 years (patient A4), and a woman aged 52 years (patient A5) attended the same church that day and subsequently developed symptoms on January 23, January 30, and February 3, respectively. *Patient A5 occupied the same seat in the church that patients A1 and A2 had occupied earlier that day (captured by closed-circuit camera)* (5). Investigations of other attendees did not reveal any other symptomatic persons who attended the church that day."

I haven't seen other examples, though, so I remain skeptical that surface transmission is a big deal. Erin Bromage previously claimed that the South Korean call center outbreak occurred "roughly 6% from fomite transfer" but then retracted the claim; not sure what happened there.

Adding a Housemate Under Covid

How socially isolated was your new housemate in their previous living arrangement? And how hard are you trying not to catch it? I'm thinking about how to minimize risk while swapping housemates in the Boston area myself, and I notice I interpret your example pretty differently if (e.g.) I imagine 'the housemate was super isolated vs. the housemate was living with an essential worker' or 'we're living with a diabetic and are trying to be ultra-cautious, vs. we're all low-risk and aren't personally worried about long-term complications if we get sick'.

Rob Bensinger's COVID-19 overview

Updates, May 8-12:


2A. Avoid people.

I recommend reading immunologist Erin Bromage’s The Risks — Know Them — Avoid Them in full. Some key claims:

  • To get infected, you plausibly need to be exposed to ~1000+ SARS-CoV2 viral particles (source) ⁠— either all at once, or over minutes or hours. The more viral particles are present, and the more time you spend exposed to them, the greater your infection risk.
  • “[T]he droplets in a single cough or sneeze may contain as many as 200,000,000 virus particles.” A single cough releases ~3000 (mostly large) droplets traveling at 50 mph (source). A single sneeze releases ~30,000 (mostly small) droplets traveling up to 200 mph (source). Smaller particles hang in the air longer. If someone sneezes or coughs, "even if that cough or sneeze was not directed at you, some infected droplets — the smallest of small — can hang in the air for a few minutes, filling every corner of a modest sized room with infectious viral particles. All you have to do is enter that room within a few minutes of the cough/sneeze and take a few breaths and you have potentially received enough virus to establish an infection."
  • In contrast, "a single breath releases 50 - 5000 droplets", most of which fall to the ground quickly; nose-breathing releases even fewer droplets (source). "We don't have a number for SARS-CoV2 yet, but we [...] know that a person infected with influenza releases about 3-20 virus RNA copies per minute of breathing" (source). This suggests that if your only exposure to an infected person is via them silently breathing on the other side of a room, it will probably take an hour or longer for them to infect you.
  • Speaking releases “~200 copies of virus per minute. Again, [pessimistically] assuming every virus is inhaled, it would take ~5 minutes of speaking face-to-face to receive the required dose” (source).
  • A toilet flush aerosolizes droplets (which might contain viable virus), so “treat public bathrooms with extra caution (surface and air)” (source).
  • “[P]lease don't forget surfaces. Those infected respiratory droplets land somewhere. Wash your hands often and stop touching your face!”
  • “We know that at least 44% of all infections — and the majority of community-acquired transmissions — occur from people without any symptoms (asymptomatic or pre-symptomatic people) (source). You can be shedding the virus into the environment for up to 5 days before symptoms begin. [...] Viral load generally builds up to the point where the person becomes symptomatic. So just prior to symptoms showing, you are releasing the most virus into the environment.”
  • “The main sources for infection are home, workplace, public transport, social gatherings, and restaurants. This accounts for 90% of all transmission events.  In contrast, outbreaks spread from shopping appear to be responsible for a small percentage of traced infections.” (source). “The biggest outbreaks are in [nursing homes,] prisons, religious ceremonies, and workplaces, such [as] meat packing facilities and call centers.” Outbreaks seem to happen disproportionately often in colder indoor environments, and at larger and more social gatherings like weddings, funerals, birthdays, and networking events.
  • “Indoor spaces, with limited air exchange or recycled air and lots of people, are concerning from a transmission standpoint. We know that 60 people in a volleyball court-sized room (choir) results in massive infections. Same situation with the restaurant and the call center. Social distancing guidelines don't hold in indoor spaces where you spend a lot of time, as people on the opposite side of the room were infected.

    “The principle is viral exposure over an extended period of time. In all these cases, people were exposed to the virus in the air for a prolonged period (hours). Even if they were 50 feet away (choir or call center), even a low dose of the virus in the air reaching them, over a sustained period, was enough to cause infection and in some cases, death.

    “Social distancing rules are really to protect you with brief exposures or outdoor exposures. In these situations there is not enough time to achieve the infectious viral load when you are standing 6 feet apart or where wind and the infinite outdoor space for viral dilution reduces viral load. The effects of sunlight, heat, and humidity on viral survival, all serve to minimize the risk to everyone when outside.”
  • You shouldn’t worry especially about “[brief visits to] grocery stores, bike rides, inconsiderate runners who are not wearing masks”. “[F]or a person shopping: the low density, high air volume of the store, along with the restricted time you spend in the store, means that the opportunity to receive an infectious dose is low.” If you have to work in a grocery store, or spend lots of time in an office or classroom — especially one with more people sharing the same space and/or air, or one that requires "face-to-face talking or even worse, yelling" — you should be much more worried.

Bromage says grocery stores aren't "places of concern", but I gather he means they’re relatively safe if you’re keeping a good distance from everyone, going when the store is pretty empty, etc. If a single cough from someone a few feet away who isn’t facing in my direction can give me COVID-19 within a few seconds, that still seems “concerning” to me!

Additionally, Jim Babcock comments on “infections while shopping appear to be responsible for 3-5% of infections”:

The source for this covers Ningbo from January 21 to March 6. My main worry, when looking at this number, is that Ningbo's mitigations may have been more effective for stores than they were for other places, in ways that don't generalize to the US. For example, I'm pretty sure they would have been screening people for fever on entry, and enforcing mask usage. I haven't been hearing of fever-screens in Berkeley (though I haven't really been out of the house), and while we do now have a mask ordinance, it's mostly cloth masks (which are less effective) and compliance doesn't seem to be very good.


The specific number for the ~1000 virus-particle claim is cited to a pretty sketchy source; it leads to a couple epidemiologists speculating with no data, and what they actually say is:

> "The actual minimum number varies between different viruses and we don’t yet know what that ‘minimum infectious dose’ is for COVID-19, but we might presume it’s around a hundred virus particles."


> "For many bacterial and viral pathogens we have a general idea of the minimal infective dose but because SARS-CoV-2 is a new pathogen we lack data. For SARS, the infective dose in mouse models was only a few hundred viral particles. It thus seems likely that we need to breathe in something like a few hundred or thousands of SARS-CoV-2 particles to develop symptoms. This would be a relatively low infective dose and could explain why the virus is spreading relatively efficiently."

So there's uncertainty of about an order of magnitude, here. On the other hand, the broader claim--that exposure size matters--is almost certainly true, and the implications of the specific number 1000 are mostly screened off by more-specific observations of which places people are getting it.

Bromage has softened the grocery store claim to “In contrast, outbreaks spread from shopping appear to be responsible for a small percentage of traced infections.”, and now cites an additional two studies for the 1000-particle claim: 1, 2.


2I. Consume 2,000-6,000 IU of Vitamin D daily, in the morning.

From Jim Babcock:

Wikipedia summarizes as "vitamin D functions to activate the innate and dampen the adaptive immune systems". Assuming that's true (I haven't verified it, and vitamin D is a subject known for attracting sketchy claims), then deficiency would lower the minimum infectious dose. On a population scale, this would be a better explanation for the infections-latitude correlation than temperature is, and would suggest that mass-distributing vitamin D supplements would be a good R-lowering strategy.


3D. Start monitoring your oxygen more often at the smallest warning sign.

[Removed or de-emphasized information suggesting hospitals will be overrun, which never really happened in the US and probably never will. This includes cutting the long Connor Flexman comment, though I still link it in the context of home oxygen concentrators.]

I now think “respiratory involvement... is the pathway by which it kills” is wrong, or at least very incomplete. I’m updating toward thinking of COVID-19 as a vascular or clotting disease at least as much as a respiratory one. Asthma isn’t a major risk factor for COVID-19 death; age, obesity, diabetes, heart disease, and hypertension are.

From the Washington Post May 10:

In the initial days of the outbreak, most efforts focused on the lungs. SARS-CoV-2 infects both the upper and lower respiratory tracts, eventually working its way deep into the lungs, filling tiny air sacs with cells and fluid that choke off the flow of oxygen.

But many scientists have come to believe that much of the disease’s devastation comes from two intertwined causes. The first is the harm the virus wreaks on blood vessels, leading to clots that can range from microscopic to sizable. [...] The second is an exaggerated response from the body’s own immune system, a storm of killer “cytokines” that attack the body’s own cells along with the virus as it seeks to defend the body from an invader.

[...] “What this virus does is it starts as a viral infection and becomes a more global disturbance to the immune system and blood vessels — and what kills is exactly that,” Mehra said. “Our hypothesis is that covid-19 begins as a respiratory virus and kills as a cardiovascular virus.”

[...] ACE2 receptors, which help regulate blood pressure, are plentiful in the lungs, kidneys and intestines — organs hit hard by the pathogen in many patients. That also may be why high blood pressure has emerged as one of the most common preexisting conditions in people who become severely ill with covid-19.

Oncologist Tatiana Prowell describes (on May 5) a Swiss autopsy series on Twitter:

[...] pathologists who did autopsies on these 21 people who died of #COVID19 think lung damage & blood clots in the smallest blood vessels (capillaries) of the lungs were the major cause of death. They found clots even in [patients] on blood thinners, which should’ve prevented them.

And quoting CellBioGuy (Apr. 13, Apr. 22):

ACE2 is expressed on endothelial cells lining blood vessels. If you get bad viremia the inner sheath of blood vessels, especially in heavily infected organs, probably just gets all messed up.

[...] The virus may be causing abnormal inflammation and a whole-body, but especially concentrated in the lungs, hyper-coagulable state that is triggering microscopic blood clots in the lungs that are one of the main contributors to morbidity and mortality and ineffectiveness of ventilation.

[...] This hyper-coagulable state might explain the reports of anomalously low oxygen measurements in people that would ordinarily indicate death or [unconsciousness]. They might have small clots in the finger the sensor is on triggering temporary sporadic low blood flow. It also could explain more of the fact that ventilators are less useful than they thought - some people going on them probably didn't actually need them.

[...] Additionally, there are two bits of immunology that explain parts of this virus's behavior and suggest ways of hurting it. First, the virus evolved in bats in which the interferon response is on an absolute hair trigger, and accordingly in human cells it almost completely escapes the interferon response. This allows it to replicate to absurd viral loads before the immune system notices it, explaining the extreme infectiousness shortly before symptoms develop. Then when the immune system notices it, it goes all out on a huge viral infection, triggering an inflammatory response that is all out of whack and can do a lot of damage. This means that it is vulnerable to inhaled interferon pretreatment ( On top of this, it may be that anything that reduces the replication of the virus in this period before the adaptive immune system mounts a robust response could reduce the probability of progression to severe disease. If antivirals work out or if chloroquine is effective (given the biochemistry I am very hopeful!), they will probably be most effective early via reducing the fraction of patients that progress to severe disease.

Second, there is evidence that the virus is able to enter and destroy (but not replicate within) T-cells using the same receptor it uses everywhere else, triggering immune suppression and altering the inflammatory profile ( It lacks HIV's obscene dirty tricks and isn't actually replicating within them, so this would be a temporary thing until recovery.


Stat reports Apr. 21:

[...] The new analysis [... suggests that] unusual features of the disease can make mechanical ventilation harmful to the lungs.

[...] “In our personal experience, hypoxemia … is often remarkably well tolerated by Covid-19 patients,” the researchers wrote, in particular by those under 60. “The trigger for intubation should, within certain limits, probably not be based on hypoxemia but more on respiratory distress and fatigue.”

Absent clear distress, they say, blood oxygen levels of coronavirus patients don’t need to be raised above 88%, a much lower goal than in other causes of pneumonia.

[...] Covid-19 affects the lungs differently than other causes of severe pneumonia or acute respiratory distress syndrome, the researchers point out, confirming what physicians around the world are starting to realize.

For one thing, the thick mucus-like coating on the lungs developed by many Covid-19 patients impedes the lungs from taking up the delivered oxygen.

For another, unlike in other pneumonias the areas of lung damage in Covid-19 can sit right next to healthy tissue, which is elastic. Forcing oxygen-enriched air (in some cases, 100% oxygen) into elastic tissue at high pressure and in large volumes can cause leaks, pulmonary edema (swelling), and inflammation, among other damage, contributing to “ventilator-induced injury and increased mortality” in Covid-19, the researchers wrote.

[...] There is a growing recognition that some Covid-19 patients, even those with severe disease as shown by the extent of lung infection, can be safely treated with simple nose prongs or face masks that deliver oxygen.The latter include CPAP (continuous positive airway pressure) masks used for sleep apnea, or BiPAP (bi-phasic positive airway pressure) masks used for congestive heart failure and other serious conditions. CPAP can also be delivered via hoods or helmets, reducing the risk that patients will expel large quantities of virus into the air and endanger health care workers.

[...] “We use CPAP a lot, and it works well, especially in combination with having patients lie prone,” Schultz said.

Assessing Kurzweil predictions about 2019: the results

Here's the context:

[...] Rotating memories and other electromechanical computing devices have been fully replaced with electronic devices. Three-dimensional nanotube lattices are now a prevalent form of computing circuitry.

The majority of "computes" of computers are now devoted to massively parallel neural nets and genetic algorithms.

Significant progress has been made in the scanning-based reverse engineering of the human brain. It is now fully recognized that the brain comprises many specialized regions, each with its own topology and architecture of interneuronal connections. The massively parallel algorithms are beginning to be understood, and these results have been applied to the design of machine-based neural nets. It is recognized that the human genetic code does not specify the precise interneuronal wiring of any of the regions, but rather sets up a rapid evolutionary process in which connections are established and fight for survival. The standard process for wiring machine-based neural nets uses a similar genetic evolutionary algorithm. [...]

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